1 / 270

Topic 1: Topic 7A Respiration

>>>>>>>>Page 2

Topic 2: Topic 7B Muscle,

Movement and the heart
>>>>>>>>Page 35

Side Lesson: Spirometer

>>>>>>>>Page 87

Topic 3: Topic 7C Control of the

Internal Environment
>>>>>>>>Page 99

Topic 4: 8A The Nervous

System and Neurons
>>>>>>>>Page 150
Topic 5: Topic 8B Coordination in
animals and plants
>>>>>>>>Page 202

Topic 6: Topic 6 Gene technology

8C
>>>>>>>>Page 240
 Topic 7A
Respiration
A2 Biology Edexcel
WBI15 unit 5

Dr. Nihal Gabr

2 / 270
17/1/2023
Part 1
ATP production
Glycolysis

Dr. Nihal Gabr

3 / 270
 Respiration
Why we need energy ;
1. Cell division
2. Muscle contraction
3. Active uptake / transport
4. Temperature regulation
5. Anabolic reactions such as photosynthesis and use to regenerate RUBP to continue Calvin cycle
6. Used to reduce GP to GALP .

Structure of ATP ( universal energy currency ) ATP is universal energy currency of all cells

1. Small , water soluble and easily transported around

the cell
2. Easily hydrolysed ( phosphate loss) to release
energy
3. Short term store of energy
Immediate energy donor in all cells as the bond between
phosphate groups is unstable and easily broken )
4. Relatively large amount of energy ( 30.5 kj / mol
5. AMP and ADP recycled to ATP , so constant
supply of ATP .
4 / 270
 Synthesis of ATP
Hydrolysis
Exothermic

ATP ………………………ADP + Pi
Condensation
Endothermic

Oxidative phosphorylation

Substrate level phosphorylation In mitochondrion

ADP and phosphorylated compound are

substrates that occupy the active site of
certain enzymes……a phosphate group
( inorganic phosphate ) transferred from the
compound to be added to ADP …to form
ATP .

Cytoplasm

5 / 270
 70S
ribosomes
Matrix
contains
enzymes for
kreb’s cycle

Inter membrane space

Stalked particles with ATP
synthase

Cristae carry the stalked particles

with ATP synthase for ATP
synthesis .

Glycolysis Cytoplasm
Linked reaction
Kreb’s cycle Mitochondria
Oxidative phosphorylation

6 / 270
 &

Inter membrane space

H+ H+ Electrical gradient
H+ H+ 5
H+Chemical gradient

· 4 ATP
Inner
synthase
membrane
2
/ Cristae

Matrix 1 H+
6
H+ 4 Energy is used to pump
hydrogen ions into the inter
NADH NAD
Hydrogen carrier Oxidised membrane space ( by active
ETC +
transport )
2 Electrons …e …pass along chemiosmosis=
electron carriers in the inner oxidative
5 Creat a proton /
membrane of mitochondrion phosphorylation
electrochemical gradient

Movement of electrons in ETC 6 H+ diffuse back by facilitated diffusion into the matrix
3
release energy through ATP synthase …..energy used to make ATP
from ADP and Pi by Chemiosmosis
ETC ( electron transport chain) 7 / 270
 Phosphorylation by chemiosmosis :

1. Oxidation of reduced NAD ( NADH) …release hydrogen atom

2. Hydrogen atom from NADH , split into hydrogen ion ( proton ) and electrons
3. The electrons pass along carriers ( from one carrier to another ) through ETC in the inner membrane of the
mitochondria
4. The energy released from electron transfer chain is used to pump proton into inter membrane space to creat a
proton/ electrochemical gradient across the cristae
5. The proton diffuse back facilitated diffusion into the matrix through ATP synthase …so the energy used in producing
ATP from ADP and Pi .

Co enzymes
Co enzyme A
NAD Non protein …assist as enzymes
Transfer acetyl
group ( 2C unit) in
Hydrogen carrier , transfer hydrogen FAD NADP Linked reaction of
In Glycolysis.
Hydrogen carrier , transfer Hydrogen carrier respiration to kreb’s
Linked reaction
hydrogen In plants cycle .
Kreb’s cycle
Oxidative phosphorylation
Kreb’s cycle
Oxidative phosphorylation
8 / 270
 Net 2 ATP
[Link] 2 NADH
2x pyruvate 3C
C6H12O6+ 6O2…………………………………………………..6CO2+6H2O+ ATP

1. Glucose move by facilitated diffusion through cell surface membrane

IN CYTOPLASM
01093850599
Glucose 6C
2. Phosphorylation of glucose by one ATP. Phosphorylation
of glucose
Glucose 6 phosphate 6C
Using 2 ATP
3. Phosphorylation of glucose 6 phosphate by another ATP molecule

Fructose 1, 6 biphosphate
( phosphorylated hexose 6C)

4. Split ( lysis )

2X Triose phosphate ( 3C )
2X TP 5. Oxidation of TP / dehydrogenation by NAD …………2 reduced NAD
So TP ( 3C compound) oxidised ….leading to reduction of 2NAD
2X intermediate bisphosphate
6. Substrate linked phosphorylation where ADP and intermediate TP ( phosphorylated compound ) occupy
active site of an enzyme and the phosphate group is transferred to ADP to form ATP …..produce 4ATP
molecules .
2X Pyruvate 3C 9 / 270
21/1/2023
Part 2
Linked reaction
Kreb’s cycle
Oxidative phosphorylation

10 / 270
 2x pyruvate ( 3C) 2. Linked reaction Dehydrogenation ….2 reduced NAD
Decarboxylation ….2CO2
Acetyl group bind to Co A …2x acetyl Co A
Cytoplasm

1
Mitochondrial matrix
1. Dehydrogenation to reduce NAD ( 2 reduced NAD produced )
2. Decarboxylation to form CO2 ( 2 CO2 produced )

2x Acetate ( 2C)

3. Transfer of 2 acetyl group to Co enzyme A

det
Co enzyme A
2x Acetyl (2C ) Co A Which delivers the acetyl group to kreb’s cycle

11 / 270
 Over all .
Glycolyis 2 pyruvate ( 3C)
T
Net LATP
2NADH
Mitochondrial matrix

1
2 x Pyruvate

=Ene
Dehydrogenation …reduced NAD x2
Decarboxylation……CO2 x2

2X acetate (2C)

It will be delivered to Kreb’s Cycle by Co A

2X Acetyl COA

Kreb’s cycle
Next page

12 / 270
 [Link]’s Cycle . 4 Dehydrogenation ..3 reduced NAD and 1
reduced FAD
2 Decarboxylation….2 Co2
Substrate level phosphorylation . X2

Mitochondrial matrix
2 B. Decarboxylation (n removal of CO2)
1 A. (2C) acetyl CO A 6C compound ( citrate) C. Dehydrogenation ( reduced NAD)
+

Oxaloacetate 4C
5C compound
C. Dehydrogenation
6
( reduced NAD)
E. Regeneration of 3 B. Decarboxylation (n removal of CO2)
C. Dehydrogenation ( reduced NAD)
oxaloacetate for cycle
to continue (at)
4C compound
4C compound phosphot
5 4C compound 4
C. Dehydrogenation
D. Substrate level phosphorylation
( reduced FAD)
Produce ATP

13 / 270
 2 carbon compound ( acetate ) was carried by CO A
Kreb’s cycle

acetyl co A …..2 carbon compound

+
4 carbon compound ( oxaloacetate )

6 carbon compound ( citrate )

B. Decarboxylation (n removal of CO2) CO2

C. Dehydrogenation ( reduced NAD) NADH

5C compound remain
CO2
B. Decarboxylation (n removal of CO2)
V2 4CO2
C. Dehydrogenation ( reduced NAD) NADH 2ATP
4C compund 6 NADH
D. Substrate level phosphorylation ATP 2FADH2
Produce ATP
FADH2
E. Dehydrogenation ( reduced FAD)
Regeneration into oxaloacetate
NADH
FAN
C. Dehydrogenation ( reduced NAD)
Oxaloacetate 226
FAD. ATP. NAD
14 / 270
 In cytoplasm
Glycolysis

Glucose ( phosphorylation two times using 2ATP )

2 NADH
Hexose 6C ( bisphosphate ) / phosphorylated 6C compound Net gain 2ATP
2 pyruvate (3C)
Split into 2 TP ( 3C compound )

Dehydrogenation of 2X TP ……intermediate bisphosphate +2NADH

Substrate level phosphorylation of ADP + 2 intermediate bisphosphate …4 ATP ( net gain 2ATP )
In matrix
Producing 2 pyruvate (3C)

Linked reaction 2NADH

2CO2
Dehydrogenation ….X2……..=2NADH
Decarboxylation…X2……..=2CO2
Producing acetyl CO A X2
Kreb’s CYCLY
6 reduced NAD In matrix
4X dehydrogenation …..3 NADH + reduced FAD
2reduced FAD
2X decarboxylation …..2CO2 10 reduced NAD
2 4CO2
Substrate level phosphorylation ….ATP 2 reduced FAD

FAN
2ATP
4 ATP

FAD. ATP.
226 NAD 6 CO2 15 / 270
 4. Oxidative phophorylation
Takes place in inner mitochondrial membrane ( cristae)
Final stage of aerobic respiration , where the energy for phosphorylation of ADP to ATP comes
from the ELECTRON transport chain
Where reduced FAD and NAD ( reduced Co enzymes ) produced from linked reaction and kreb’s
cycle are oxidised

[Link] co enzymes NAD FAD

transport hydrogen to the ETC

L
ixjx

[Link] of the reduced NAD and FAD to release hydrogen atom

2. The hydrogen from Co enzymes is split into hydrogen ions and electrons
3. These electron will pass across carriers in the ETC ( from carrier to carrier ) in the inner mitichondrial
membrane to reach the Cytochrome oxidase complex .
4. The energy released from electron transfer is used to pump protons ( by active transport) into inter-membrane
space to creat a proton gradient across the cristae
5. The hydrogen ions then diffuse back by facilitated diffusion into the matrix through ATP synthase.
ATP is produced from ADP and Pi 9 phosphorylation of ADP)
6. Oxygen act as the final electron acceptor ( Oxygen , proton , electrons together form molecules
water ) ..oxygen is reduced to water….catalysed by cytochrome oxidase ( protein in the inner mitochondrial
membrane ) 16 / 270
Role of oxygen in aerobic respiration

Oxygen is needed in oxidative phosphorylation

Oxygen act as a final electron acceptor
From electron transport chain
Reduced to water / accepts the hydrogen ion ( from reduced NAD / FAD) to form water
For regeneration of NAD and FAD
And so the electron transport can continue Cytochrome oxidase responsible for OXYgen

For the production of ATP

reduced to water

In absence of oxygen ,

Cyanide causing rapid death

Non competitive inhibitor
Inhibit the enzyme ( cytochrome oxidase ) responsible for adding hydrogen to oxygen to
form water
Where oxygen act as a final electron acceptor
Hydrogen ions and electrons accumulate on the carriers
So ETC will stop
No pumping of hydrogen ions …so no proton gradient
No proton diffuse back through ATP synthase
So less / no production of ATP
No chemiosmosis and oxidative phosphorylation …..ATP only from glycolysis 17 / 270
Respiration without oxygen

There is insufficient supply of oxygen ( the final electron acceptor)

The final reaction pf oxidative phosphorylation doesn’t take place
The regeneration of NAD is stopped
Where there is no way for the reduced carriers ( reduced NAD and reduced FAD) to be oxidised
So Kreb’s cycle and linked reaction will stop as they lack NAD and FAD
A
Lactate feremntation
So the regeneration of NAD is achieved by the PYRUVATE molecule from glycolysis …accept
hydrogen from reduced NAD in process FERMENTATION

Glucose
Glycolysis …..( steps + substrate level phosphorylation )

2XPyruvate (3C)
Cant enter the mitochondria so remain in the cytoplasm
Pyruvate will be reduced ( hydrogen acceptor )
In cytoplasm
By reduced NAD from glycolysis
Reduced NAD will be oxidised ….to be regenerated …to be available to convert / oxidise 3C sugar to pyruvate
So ATP production will continue from glycolysis

Lactate ( 3C) …energy rich

+ net gain 2 ATP Lactate moves out of cells into blood to be transported to liver 18 / 270
Fate of lactate 2x Pyruvate x2

Lactate diffuse into the blood oo NADH

NAD
NADH
NAD hegre
>

To be transported to liver
L

2x Lactate
Where lactate is converted back into pyruvate
Involving the production of reduced NAD
So pyruvate is then oxidised

Through Kreb’s cycle (Where pyruvate enter the linked reaction to react with CO A / respired)
Using oxygen debt / requires extra oxygen
Producing Co2 and water

Glycolysis
2ATP
2NADH
Anaerobic respiration
Glucose INAD.
2 pyruvate

2NADH
Linked reaction
>
2 NADH
Pyruvate

8freeLactate
2 Co2

2FADH2
cone
inRus
Kreb’s cycle 2ATP
6NADH
4CO2

Oxidative phosphoryaltion

O2 + H+ + e-..water 19 / 270
24/1/2023
Part 3
Anaerobic respiration
Respiratory substrate
Respiratory quotient

Dr. Nihal Gabr

20 / 270
 Aerobic respiration Anaerobic respiration
Glycolysis
Glycolysis
2ATP
2NADH
2 pyruvate

Glucose
2x Pyruvate x2
Linked reaction
2ATP
2 NADH

NADH
2NADH

NADH
2 Co2

2X Pyruvate
Kreb’s cycle
2FADH2
2ATP
6NADH
2NADH
Reduction to pyruvate
NAD NAD &chic
4CO2 152NAD
2x Lactate
Lactate
Oxidative phosphoryaltion
O2 + H+ + e-..water
To the liver

②NARApH Oxidation

Pyruvate

Aerobic respiration

CO2 and water

21 / 270
 Aerobic respiration

C6H12O6 + 6O2 ……..6CO2 + 6H2O+ ATP

10 NADH….30 ATP
Glycolysis…..cytoplasm 2FADH2,…..4 ATP
Joxidph.
Glucose …….2x pyruvate 2 ATP ….
2NADH 2ATP ….. Sub. levelph.
2ATP

Linked reaction…..matrix 38ATP

2x Pyruvate …. 2 acetyl COA

2CO2
2NADH

KREB”S CYCLE…..matrix

2 acetyl CoA + oxaloacetate ……..oxaloacetate

2 FADH2
2ATP
6NADH
4CO2
Oxidative phosphorylation
NADH …3ATP
10 NADH, 2 FADH2……….1/2 O2 + 2e+ 2 H+…H2O
FADH2….2 ATP 22 / 270
Lactate fermentation
( anaerobic respiration )

C6H12O6…….2 C3H6O3 + 2 ATP

Glycolysis…..cytoplasm

Glucose …….2x pyruvate

2NADH
2ATP

Reduction of pyruvate ( hydrogen acceptor ) to allow regeneration of NAD ,

for glycolysis

Reduction
2X Pyruvate …………………….2 x lactate ( reduced form of pyruvate )
NADH ….NAD

2X Lactate ……………………….2
Oxidation x pyruvate ( oxidesed form of lactate )
NAD ….NADH
Using oxygen from oxygen debt
Linked reaction…..matrix

2x Pyruvate …. 2 acetyl COA

2CO2 Aerobic
2NADH

KREB”S CYCLE…..matrix
respiration /
2 acetyl CoA + oxaloacetate ……..oxaloacetate

2 FADH2 oxidation of
2ATP
6NADH
4CO2
lactic acid
Oxidative phosphorylation

10 NADH, 2 FADH2……….1/2 O2 + 2e+ 2 H+…H2O

CO2 and water 23 / 270
B
Alcohol feremntation C6H12O6 …………2CO2 + 2 C2H5OH + ( ATP)
Irreversible ( yeast and in plants mainly roots)
Glucose
Glycolysis
2 NAD
2NADH
Pyruvate

Ethanal (acetaldehyde )
Act as hydrogen acceptor from reduced NAD

Irreversible reaction
NAD+ regenerated , so can accept hydrogen so glycolysis can continue
Ethanol

24 / 270
 Alcohol fermentation Lactate feremntation

Ethanol produced Lactate produced

Irreversible ( convert
Reversible ( lactate can be converted
pyruvate into ethanol )
into pyruvate using oxygen debt )

Ethanal act as hydrogen acceptor

Pyruvate act as hydrogen acceptor

Involved decarboxylation producing CO2

X

Dosen’t need oxygen

Needs oxygen ( oxygen debt)

25 / 270
Why anaerobic respiration produces less ATP

1. Only glycolysis taking place ( which involves substrate level phosphorylation )

Producing only 4 ATP with net gain 2 ATP
2. Oxygen is absent which act as final electron acceptor
So ETC doesn’t take place
Where most of the ATP produced in oxidative phosphorylation under aerobic conditions
3. Pyruvate is converted to lactate which is energy rich
4. Some reduced NAD is used to reduce pyruvate to lactate rather than entering ETC .

If a runner starts long distance event at a fast speed , then he will have to slow down to speed that is supported by
aerobic respiration, why?

[Link] one can tolerate the high concentration of lactate that will be produced from anaerobic respiration when
running ata fast speed .
2. No enough glycogen stored in body to provide the glucose for such s Long time .
3. Fats can only be respired aerobically

Oxygen debt Oxygen consumption after exercise increase to repay the oxygen debt

The volume of oxygen absorbed by the body to metabolise the lactate produced from anaerobic respiration in
muscles .
Where it is responsible for the conversion of lactate into pyruvate in a reaction catalysed by lactate dehydrogenase .

26 / 270
Explain why after stopping exercise the oxygen consumption increases :

1. As lactate was produced from anaerobic respiration

2. So oxygen is needed to metabolise ( reoxidise ) the lactate .
3. Where its resposnible for the conversion of lactate into pyruvate

So that glycogen stores are replenished in muscles

Also reoxygenation to haemoglobin and myoglobin

Also oxygen is needed in aerobic respiration .

Used in oxidative phosphorylation to allow regeneration of NAD .

Explain increase in lactate concentration during exercise :

Muscles using oxygen faster than it can be delivered

Anaerobic respiration is taking place
Pyruvate converted into lactate
And reduced NAD is oxidised

27 / 270
 Respiratory substrate

Glucose is the essential respiratory substrate for the cell …….yet other cells can oxidise / break down lipids and
amino acids .
The substance used as a fuel and oxidised during cellular respiration
to produce ATP for energy

16 kj /g

39 Kj /g
17kj / g

Why lipids has the highest amount of energy per unit mass ?

Fatty acids have more hydrogen per unit mass

More reduced NAD and FAD produced
More Electron pass along ETC
More hydrogen ions pumped out into inter membrane space
Creating a steeper proton gradient
So more ATP produced per unit mass
So Fats are only broken AEROBICALLY , so more hydrogen ion transferred for ETC for more
chemiosmosis .
28 / 270
1. Glucose
The main respiratory substrate.

2. Lipids
They have a high energy storage
Lipase
Lipids ……………………………….fatty acids +
• fatty acids …are made from a long hydrocarbon chain where they will be broken down an enzyme …where 2
carbons are broken at a time producing acetyl CO A
• Acetyl COA will enter matrix
• And used in Kreb’s Cycle which produce ATP

The hydrogen in the hydrocarbon chain is split ..electron are accepted by electron carriers to pass by electron
transport chain to produce ATP .
We use the lipids only in the absence of glucose .

29 / 270
3. Proteins

Protein broken down into amino acids

Where deamination takes place in liver that involves the removal of amine group
The remaining organic part is converted into Pyruvate or acetyl CO A ..depending
on the R groups
Then enter kreb;s cycle
- protein is used as respiratory substrate in absence of glucose and lipid
-in case of starvation or hibernation .

Excess amino acids …..

a
Win
ve
"cubivalen

30 / 270
Respiratory quotient

Glucose …RQ = 1
Triglyceride …..RQ= 0.7
Proteins ……..RQ= 0.9

1 or less than 1 ……respire aerobically

More than one ( mixture )
No O2 ….anaerobic respiration …RQ is infinity

31 / 270
Structure of mitochondrion

1. Outer mitochondrial membrane

2. Inner mitochondrial membrane ;
Folded forming cristae to increase surface area
A) contain ATP synthase ( for oxidative phosphorylation)
B) site of ETC
Involves pumping of Hydrogen ions / protons into inter membrane space
So it will build up a proton gradient
Protons will diffuse back through ATP synthase into matrix
Making ATP
.Not permeable to glucose / nor hydrogen ions ( they cant pass through hydrophobic core) .

3. Inter membrane space : low pH as its site with high proton concentration

4. Matrix : site of linked reaction and Kreb’s cycle , it contains DNA loop and 70S ribosomes .

5. DNA : has genes for transcription …..coding for mRNA to code for proteins such mitochondrial enzymes
( ATP synthase)

6. 70 S ribosomes : site of translation , assemble amino acids into proteins such as respiratory enzymes /
inner membrane proteins . 32 / 270
 Check list
[Link] the uses of energy
2. Describe the structure of ATP ( recognise )
3. Why ATP is considered as universal energy currency
4. 2 Methods of synthesis of ATP ( substrate level phosphorylation and oxidative phosphorylation)
5. Draw a mitochondria with labels
6. Describe the function of different parts of mitochondria .
7. Describe steps of oxidative phosphorylation by chemiosmosis .
[Link] 3 Co enzymes playing a role in respiration
9. Describe steps of both glycolysis , linked reaction and place of each
10. KREB’s cycle : site cycle taking place , the products
11. Write in details all steps of Oxidative phosphorylation
12. State the role of oxygen in aerobic respiration
13. Explain why cyanide act as respiratory poison
14. Describe steps of anaerobic respiration ( lactate fermentation )
15. Why anaerobic respiration produces less ATP
16. If a runner starts long distance event at a fast speed , then he will have to slow down to speed that is supported
by aerobic respiration, why?
[Link] whats oxygen debt .
18. Explain why after stopping exercise the oxygen consumption increases ?
33 / 270
10 Respiratory quotient (RQ):

• The respiratory quotient is the ratio between the volume of carbon dioxide produced in
respiration and the volume of oxygen absorbed: C6 H12O6 + 6O2 …..6CO2 + 6H20
• 5
In unit time
In unit time

• If the RQ is less than 1 or equal to 1 , respiration. Is aerobic .

• If no oxygen absorbed, then no aerobic respiration is occurring at all and RA is infinity (. ) .
• RQ values higher than 1 indicate a mixture of aerobic respiration and ethanol fermentation in
yeast and plants.

• The values of RQ of carbohydrate , lipid and protein can be calculated from equation that
show their complete oxidation.

r
• This is the equation for aerobic respiration of glucose.

ab
Affected by respiratory
-
-

substrate
• The ratio between oxygen and carbon dioxide is 1:1 , so the RQ is 1.
lG
• This is the equation for the aerobic respiration of a triglyceride:
iha
-

• The RQ for tristearin=

=
• The equation for the aerobic respiration of amino acids ( minus the amino acid
.N

group removed by deamination) is :

Dr

• RQ values are useful as they tell us whether respiration is aerobic or not , and the
type of substrate that is respired (e.g carbohydrate , lipid or protein) or the likely
mix of substrates.

Metabolism of lipids….

[Link] Gabr 34 / 270

22
 Topic 7b
Muscle , movement and
the heart
A2 Biology Edexcel
WBI15 unit 5

Dr. Nihal Gabr

35 / 270
28/1/2023
Part 1
Joints , tendon ligaments
Antagonistic muscle
Structure of muscle
Types of muscle fibres

36 / 270
The skeletal tissues ( bone ) Read

A
Bone cells ( osteocytes ) fixed firmly in a matrix of collagen and calcium salts
Strong , hard yet light to help to move about .
Compact bone is dense and heavy ..found in long bones of your body .
Spongy bone has much more open structures so much lighter ( found in pelvis and head of femur )

Cartilage : made from chondrocytes within a matrix of collagen fibrils

Being elastic ( stretches and returns to its original size )
Able to with stand compression forces ( shock absorber )
Found between bones Hyaline cartilage
Types of cartilage
A) hyaline cartilage : found at the end of the bones ( articular surfface of
bones) ( and in nose , air passage ways and parts of the ear)
B) white fibrous cartilage : has densely packed collagen in matrix with great
tensile strength but less flexible than other forms of cartilage
Forming discs between ur vertebrae and found between bones in the joints

37 / 270
 Structure of joint

Its a place where two or more bones meet …allowing different parts of the skeleton to move

B
Joined by ligaments

Contain synovial fluid

1. Reduce friction
[Link] friction 2. Act as a shock
2. Lubricates the joint to absorber
facilitate movement .
1. Attaches a bone to bone
Hold the bones together to avoid
1. Attaches muscle to a bone . dislocation.
2. No elastic fibres ( non elastic ) so dot 2. Elastic fibres to be elastic
stretch ( stretch ) so bones can move at the
As their function is join muscle to bone , so joint without dislocation.
they allow the transfer of the pull action 3. Have collagen to provide
( force ) of muscle to the bone strength .
So bone is moved .
3. Mostly made from white fibrous tissue
( full of collagen to be inelastic ) . 38 / 270
 Flexion Straightening Extension
Muscle how they work Bending
Flexor

C
[Link] muscles work in pairs
2. Called antagonistic pairs Extensor
3. They work opposite to
each other
[Link] one contract the
other relax
As muscles pull but never Moving forearm upwards Moving forearm downwards
push
[Link] Bend at the elbow joint Straightening ( extensor)
muscles which
extend at a joint [Link] ( flexor muscle ) contract and 1. Triceps ( extensor ) contract and
2. Flexors are shorten ' become shorter
muscles that [Link] ( extensor muscle ) will relax
bend or flex at a 2. Biceps ( flexor ) relax and become
and flatten
joint longer / thinner / flat
3. Working antagonistic to each other.
3. Working antagonistic to each other.
4. So tendons ( attaching muscles to
4. Tendon ) attaching muscle to bone 0
bones ) transfer the force ( pull action of
transfer the pull action of the triceps
biceps) and cause the arm to bend at the
causing forearm to be lowered
joint …raise the forearm.
And arm straightened

39 / 270
 Triceps ( extensor )
Biceps ( flexor )

Contract
Relax Flexor
Straightening
Extensor

r
ab
lG
Extensor muscle contract and shorten
Flexor muscle relaxes
Leg is straightened
ha
Where they work antagonistically , when one contracts the other relaxes
Where the flexor is stretched
With tendons attaching muscle to bone
.Ni

To transfer the force of the extensor to the bone to straighten the leg
Dr

Flexion Extension
Bending Straightening
Biceps ….responsible for Triceps …responsible for
bending = flexor straightening = extensor

D r. Nihal G abr
40 / 270
-

41 / 270
Muscle structure

D
Muscles have a good blood supply ..to be provided with glucose and oxygen for cellular respiration
Where it supplies muscles with ATP needed for contraction
Respond to nervous system stimulation and chemical stimulation from hormones as adrenaline
Three types
1. Skeletal muscles
2. Smooth muscles ( involuntary . Not striped , under control of involuntary nervous system ) in gut and in
blood vessels
3. Cardiac muscle in heart , striated with special cross connections
Contract spontaneously ( not needed to be stimulated by either nerves or hormones )

Muscle fibre has many myofibrils

Lie // to each other
Made from sarcomeres
Sarcomere made from actin and myosin

Myofibril

42 / 270
 Thin filament ( actin)
Muscle
Troponin
structure :
Globular protein
Striated strips
Muscle fibres are made from
1. Myofibrils Tropomyosin Long thin thread

MYOFIBRILS lie // to each other of fibrous protein

each Myofibril made from SARCOMERES Myosin head

SARCOMERES have actin ( thin ) filament and myosin ( thick )
filament .

2. Sarcolemma ( cell surface membrane )

3. Sarcoplasm ( cytoplasm )
4. Many mitochondria in sarcoplasm
5. Sarcoplasmic reticulum ( which stores and release calcium ions )

43 / 270
44 / 270
31/1/2023
Part 2
Types of skeletal muscles
Muscle contraction
SAN and AVD

DR. Nihal Gabr

45 / 270
Myoglobin

Pigment with high affinity for oxygen found in the muscle

So readily accepts oxygen from blood .
And act as oxygen store in the muscles

Types of skeletal muscles

Aerobic ( oxygen supply ) Anaerobic

Slow twitch muscle fibres Fast twitch muscle fibre

There are two types of skeletal muscle fibres in mammals with different level of performance
Most muscles contain a mixture of the two types of fibres
Balance will affect the performance and the color of the muscle .

Fast twitch fibres Fatigue quickly

Slow twitch fibres Fatigue resistant
Adapted for steady action over a period of time
Contract slowly ……..long period Contract more rapidly ..short period
[Link] capillary density …..ensuring a good supply of oxygen and glucose 1. Less capillary density
2. More myoglobin allowing more oxygen storage
2. Less myoglobin
3. Many mitochondria to allow more aerobic respiration to produce more ATP
3. Few mitochondria
4. Smaller capacity of sarcoplasmic reticulum
5. Less glycogen ( rich in blood supply ).
4. larger capacity of sarcoplasmic reticulum
6. Deep red colour ( blood supply and myoglobin) 5. More glycogen
7. More ATP ( aerobic respiration) 6. Paler color
7. Less ATP ( anaerobic respiration ) 46 / 270
 Explain why muscle fatigue rapidly
occurs ?

[Link] supply is limited

2. Due to anaerobic respiration and
production of lactate which build up .
3. Cause a decrease in pH
4. Which in turn affects the enzymatic
activity / prevent muscle contraction .
5. Thus slowing down glycolysis / ATP
Similarities
production
Contain actin , myosin , tropomyosin, troponin
6. So affecting muscle contraction .
Consist of sarcoplasm , sarcolemma , sarcomeres .

Differences
Slow twitch muscle fibres Fast twitch muscle fibres

More mitochondria Fewer mitochondria

More myoglobin Less myoglobin
Less glycogen More glycogen
Less creatine phosphate More creatine phosphate

47 / 270
Muscle contraction

Z line at the middle of every i band

Sarcomere is the adjacent distance
between 2 z lines .

↑....... Myosin head binds to actin when ADP is

light heavy. ADP attached to the head ..release of ADP cause the
motion /tilting of the head + actin move + power
stroke

↑.......
x/ ATP bind to myosin head ..cross bridge broken
ATP
X
…ATP hydrolysed releasing energy ..so head
return back to original position

48 / 270
Summary to understand
1. Calcium ions ( released from the sarcoplasmic reticulum )
bind to troponin
Troponin changed its shape
Cause the movement of the tropomyosin which exposes the
binding site of myosin head on the actin filament ..( ADP is
attached to the myosin head means head is at state to bind to
actin filament and form a cross bridge ) .

[Link] allows the myosin head attach to the actin filament

forming actomyosin bridge. ( actomyosin)

[Link] attached to actin filament , myosin head change their

angle / tilt ..pulling the actin filament along towards the center
of sarcomere ……with the release of ADP molecule causes
the change in shape of myosin .

4.A molecule of ATP again attaches to the myosin head ,

causing detachemnet of myosin head from the actin
filament and change its shape .

[Link] this ATPases in myosin head are activated by the calcium ions released by
-

SR
ATPases catalyse break down of ATP attached to myosin head , this allows the
myosin head to return back to normal position .
-

[Link] myosin head now are detached and can attach to another binding site on actin filament and repeat the
process 7. The process results in Actin is pulled past / across the myosin where sarcomeres shorten .
As the filament slide past one another , it causes the sarcomere to shorten ..process called sliding filament
49 / 270
model
 ATP
Summary to study 1. Head leave actin and return back to
normal position/ breaks the cross
bridge / detach myosin head
1. Calcium ions ( released from sarcoplasmic reticulum ) 2. Active transport of calcium ions
2. Bind to troponin
3. Troponin changed its shape causing the movement of the tropomyosin which exposes the binding site of
myosin head on the actin filament .
4. This allows the myosin head to attach to the actin filament forming actin myosin bridge
5. Actin is pulled past / across the myosin ( by sliding filament model ) where sarcomere shorten
6. The bridge breaks and the process is repeated 50 to 100 times per second
7. The shortening of myofibrils together results in contraction of muscle

*
Explain the role of calcium ions in muscle contraction
Explain the sliding filament model
Explain muscle contraction

Muscle relaxation :
Sarcoplasm fc7t Sarcoplasmic
1. Calcium ions are actively transported back into SR using ↓ reticulum

energy from hyrolysis of ATP

2. This reabsorption of calcium ion allows the tropomyosin Myofibril

to block the actin filament again .

3. Myosin heads are unable to bind actin filaments and
coordination stops ( muscle relax) . Hydrolysis of ATP
N
ATP ase in head of myosin
50 / 270
4/2/2023
Part 3
SAN and AVN ( regulation of the cardiac cycle )
Stimulation of the increase in heart rate

51 / 270
The cardiac cycle : 0.8S

Diastole Atrial systole Ventricular systole

0.4 S 0.1 S 0.3 S

Relaxation of the heart muscle CONTRACTION OF BOTH ATRIA CONTRACTION OF
• Atria and ventricles are relaxed [Link] are relaxed BOTH VENTRICLES
( filling of the heart ) . [Link] of atria decrease Atria relax
• atrioventricular valve is open …. and blood pressure in atria Ventricles contract
to allow filling of the heart where increase Atrioventricular valve closed
blood flow from vein through 3. Atrioventricular valve Semilunar valve open
atria to the ventricles open
• Semilunar valves closed …. 4. Blow flow into ventricles
where the pressure of the blood 5. Semilunar valve closed
in ventricles decrease , causing
SAN act as a pace maker
a slight back flow of blood where
Initiate depolarisation
blood fill the semilunar valve Send waves of excitation to the muscles in
cusps causing them to close . atrial walls ….cause atrial systole

Heart muscle is myogenic

Stimulation generated within the muscle ( contracts
without an external stimulus )
Resulting depolarisation 52 / 270
Cardiac muscle is myogenic
AVN
SAN Found in the septum
Delay waves of excitation / depolarisation
1. Initiate depolarisation
1. Relay impulse
2. Acting a pacemaker ( act rhythmic
2. Receive waves of excitation and send them to bundle
contraction )
of his and then purkyne tissue by time delay of 0.1 S
3. Send of waves of excitation across the
3. Ensuring that atria contract before ventricles
muscles in atrial walls 4. Where the bundle of His and purkyne tissue spread
4. Stimulate both atria to contract ( atrial waves of excitation down to the base of the septum /
systole ) apex of the heart then spread them upwards across
5. Atrioventricular valves open the muscles in ventricular walls ..as both ventricles
Blood is forced into the ventricles contract from base and upwards
With semilunar valves being closed . 5. Thus helping squeeze the blood up into the arteries53. / 270
54 / 270
Electrocardiogram ? Ventricular systole

1. It shows heart Ventricular diastole

rate / heart
Atrial systole
rhythm / waves Ventricular
depolarisation
2. As these are the Ventricular
diastole
waves of electrical Atrial
( ventricular
activity in the heart depolarisation repolarisation )
3. Over a period of ( excited )
time or cardiac
cycle
Impulses
leave
SAN.

PR interval

55 / 270
P wave QRS complex T wave
56 / 270
57 / 270
 Atrium

:
Ventricle

i
Aorta

Atrial systole
0.1 S
Ventricular systole Diastole
0.4 S
0.3 S

58 / 270
7/2/2023
Part 4
Homeostasis

59 / 270
 Homeostasis
Maintenance of the physiological conditions inside the body at near constant level despite the
changes in the environment and in then body ….by negative feed back mechanism ( mechanism
that returns a change away from the normal valve back to normal value to ensure a constant
value / set point .

Explain the importance of homeostasis

1. Regulating core body temperature : low temperature slow down the rate of metabolic reactions and at
higher temperature, protein molecules including enzymes will denature and can’t perform their functions.

2. Blood glucose concentration : ;lack of glucose concentration in blood , cause slower rate of respiration ,
so less energy available for cells . And higher glucose concentration in blood , lower the water potential of
blood causing the water to move out of the cells so thy shrink and less water available for metabolic
reactions

3. Water potential of blood : lower blood water potential so water leave the cells so affect metabolic
reactions and higher water potential of blood will cause more water to enter the cells so they burst

Temperature , blood glucose concentration , pH , metabolic rate ,water potential have to be regulated

60 / 270
Set point / norm The desired level

Receptors Monitor the set point ie detect the deviation from set point ( detect internal external stimuli )

Effector Muscle or gland , carry a response to return the system to the set point / norm thus creat a

Feed back loop Inform the receptors returned to the norm ( action taken by the receptor )

61 / 270
 Negative feed back :

Receptors detect a change in condition …effectors will be stimulated to restore the norm / equilbrium
state
Negative feed back mechanism
1. Changes in the factor away from set point act as stimulus ( Where pH of the blood needs
to be kept within a narrow range ).
2. Detected by receptors
3. Cause a release ( from coordination center) of nerve impulse or hormone
4. To reach to target organ ( effector )
5. Effector perform a correction action
6. Factor returns back to norm / set point

Positive feed back :

Stretch receptors in
cervix send impulses to
brain
Positive feed back results in an increase in the
change ( of the variable )

Negative feed back results is a decrease in the

change ( of the variable )

62 / 270
 Controlling heart rate and breathing rate during exercise

Cardiac out put = stroke volume x heart rate

Volume of the blood pumped by the heart per beat

3 Chemoreceptors/ 2
baroreceptors Send
Cardiovascular control system in medulla oblongata impulses through
sensory neurones to

. Describe how the 1

Send nerve impulses changes in heart rate 1. Change in blood pH ( due
to SAN across
is coordinated / to increase in CO2 /
4 stimulated as the lactate in blood )
person exercise
Detected by chemoreceptors
active level
increases . in the carotid artery and aorta.
Parasympathetic
Sympathetic 2. Change in blood pressure
nerves detected stretch receptors
nerves
( baroreceptors ) in carotid
Inhibit SAN
Stimulate SAN artery and aorta
By releasing nor epinephrine / epinephrine By releasing Acetyl choline
Generate more impulses per second Generate less impulses per second
SAN excitation rate increase
SAN excitation rate decrease
Heart rate increase / increase blood
Heart rate decrease. 5
flow to lungs Change in heart rate and heart volume affects
Vasoconstriction. 5 Vasodilation in blood vessels
blood pressure and blood chemistry 63 / 270
Describe the changes in heart that cause an increase in cardiac out put .

Increase in heart rate

Increase in stroke volume Cardiac out put = stroke volume x heart rate
Increase in the activity of SAN
The time delay from AVN decreases
The ventricles contracts more forcefully

Chemoreceptors A) In case of how increase in heart rate is stimulated

1. Sensitive to levels of CO2 in blood
2. Found in AORTIC body / aorta and carotid artery / artery + medulla
3. As CO2 concentration increase …..blood pH decrease …..the chemoreceptors detect the decrease in
pH …..so send impulses across SENSORY NEURONES to cardiovascular center in MEDULLA
OBLONGATA…….to send more frequent nerve impulses down sympathetic nerve to heart ( SAN) …by
releasing nor epinephrine …..so SAN send more waves of excitation ………increase heart rate /
increase blood flow to tissue / lungs ..increase oxygen supply to tissues ………….more CO2 is removed

In case of how decrease in heart rate is stimulated

#
When chemoreceptors in AORTA and carotid artery detect the increase in pH …back to normal
Stimulate../ send impulses to Cardio vascular center in medulla oblongata
So send more nerve impulses via parasympathetic nerve
To the SAN
Thus slowing down waves of excitations from SAN
64 / 270
 What stimulates the increase in heart rate during exercise 5. Nor adrenaline /nor
[Link] increase in CO2 epinephrine released onto
concentration in blood due SAN
to increase in rate of aerobic
respiration / increase in
lactate Chemoreceptors
6. The SAN is
N
Through

stimulated to send
sympathetic and
parasympathetic

2. Blood pH in lowered , Send more frequent nerve more waves of

impulses to stimulate SAN
detected by chemoreceptors Send more frequent nerve excitation across the
in the aorta and carotid walls of the heart
impulses to slow down SAN

artery / and in medulla

3. Send nerve impulses 7. Increasing

across the sensory heart rate / blood
neurones to cardiovascular supply to tissues
center in the medulla . and oxygen
supply / rapid
4. Then more electrical removal of CO2 .
impulses sent from the
medulla to the SAN through
sympathetic nerves
65 / 270
Baroreceptors In walls of carotid artery and aorta
In carotid artery in neck and aorta
…sensitive to pressure changes
1. Heart rate is still high
2. increase Blood pressure in arteries
3. Caused baroreceptors stretched
4. They will send nerve impulses through sensory neurone
Stopped
5. To CV center in medulla oblongata
6. Which inturn send more frequent impulses across the parasympathetic
nerves …acetyl choline
7. To slow down heart rate and vasodilation in blood vessles
8. So decrease in blood pressure again

[Link], low heart rate

2. Decrease in blood pressure
3. Reduce stretching on baroreceptors
4. Reduce stimulation from these receptors to the CVcenter
5. CVs send nerve impulses across sympathetic nerves to the
( SAN ) in the heart ….through nor epinephrine
6. Increase heart rate and blood pressure ( by constriction)
66 / 270
 Baroreceptors

1. Anticipation to exercise
Stopped
2. Adrenaline is released
3. Blood vessels are already dilated ( vasodilation) …at the beginning of exercise

Blood pressure fall / decrease / low

i Reduce stretch on the baroreceptors so almost stop responding

( reduce their stimulation).
Exercise

&
Cardiovascular center immediately send
signals along sympathetic nerves to stimulate
heart rate and increase in blood pressure again

When exercise stops , So baroreceptors stretch CV center respond to send more nerve impulses
again as blood pressure increases, heart across the parasympathetic nerves to slow down
continues to pump harder and faster. heart rate and because vasodilation in blood
vessels so lowering blood pressure again 67 / 270
 oh pansym
tormone Ach.

[Link]
↓
serious
SANWamchexe
love H.R

LOWeT. P

dow
Kiluted or
SCO* oin-sEmNretirement
Hansia on borocept.

68 / 270
The change in breathing rate and depth is coordinated 4 volumes

Tidal ( VT)
Residual

21
Expiratory reserve volume (ERV)
IRV Inspiratory reserve volume ( IRV)
VT
ERV 4 capacities ( summing up 2 or more of volumes )
RV Vital capacity
Total lung capacity
Inspiratory capacity
Functional residual capacity

Vital capacity ; IRV + VT + ERV

Total lung capacity = VC + RV
IC = VT + IRV

69 / 270
Extra air breathed
out ( deep breath out)

70 / 270
 Resting breathing

1
Ventilation center in medulla
( inspiratory center which controls breathing in ) 4
( expiratory center ( control breathing out forceful ) These impulses inhibit
Send impulses the Ventilation center
across the
which inn turn stop
stimulating the
sympathetic nerves breathing muscles

Send impulses to
To intercostal muscles and ventilation center
5
diaphragm
2 To contract ( inhalation) So you stop
breathing in

3
Stretch receptors ( control Muscles relax
the resting breathing rate ) Exhale
Lungs inflate In walls of bronchi
6
Send impulses

Air in
Filling lungs

71 / 270
How increase in breathing rate and depth in coordinated during exercise

3
Send back impulses to the Send back impulses to the
Ventilation center in 3
main ventilation center
medulla main ventilation center

( inhibit) ( stimulate)

l
4
4
Inhibit the breathing Stimulate breathing
muscles , Impulses are
2
muscles, Impulses
sent out to the are sent out to the
2 breathing muscles breathing muscles
Chemoreceptors in
Chemoreceptors in ( effectors ) so ( effectors ) so
carotid arteries and breathing rate carotid arteries and
breathing rate
aorta ( carotid bodies decrease and aorta ( carotid bodies
increase and
and aortic bodies) and in breathing shallower breathing deeper and aortic bodies) and in
medulla medulla
Detect increase in pH Detect decrease in pH

1
Blood pH normal '
1
Increase in pH Co2 normal
oxygen meet body If CO2 Decrease in pH
Decrease in Co2 If CO2 demand Increase in Co2
Increase in oxygen level rises
levels fall Decrease in
oxygen

72 / 270
 How increase in breathing rate and depth in coordinated during exercise

Summary

1. Increase in CO2 concentration in alveoli so increase CO2 concentration in

blood .
2. Increase in lactate produced from anaerobic respiration
3. Decrease the blood pH
4. Detected by chemoreceptors
5. In carotid body / aortic body .
6. Stimulate the ventilation center in medulla
7. Which in turn send more frequent impulses along the neurones
8. To the intercostal muscles and diaphragm
9. To contract more frequently
10. Increasing both breathing rate and depth

73 / 270
Check list
1. Explain the function of tendons and ligaments
2. Explain how muscles work to straighten leg / bend leg
3. Explain how muscles work to straighten ur arm at the elbow / bend with an angle at the joint
4. Explain whats meant extensors and flexor
5. Describe the structure of muscle fibres
6. Explain the importance of myoglobin
7. Compare and contract between fast twitch fibres and slow twitch fibres
8. Explain why fast twitch muscle fibres fatigue rapidly occurs ?

9. Explian how the cardiac cycle and sequence of muscular contraction in heart is coordinated .
10. Explain the role of SAN
11. Explain the role of AVN
12. Describe what’s an ECG.
13. Label the waves on the ECG
14. Define homeostasis .
15. Describe the feed back mechanism
16 name and describe a positive feed back mechanism
17. Describe the changes in heart that cause an increase in cardiac out put .
18. Describe how the changes in heart rate is coordinated / stimulated as the person exercise
active level increases . 74 / 270
19. State the role of chemoreceptors in stimulating heart rate
20. What stimulates the increase in heart rate during exercise
21. How increase heart rate is stimulated
22. State two other factors stimulating change in heart rate
23. Explain the role of baroreceptors during exercise .
24. Define
Tidal ( VT)
Residual
Expiratory reserve volume (ERV)
Inspiratory reserve volume ( IRV)

Vital capacity
Total lung capacity
Inspiratory capacity

25. Identify each on trace of spirometer

26. Describe how breathing rate is maintained
27. How increase in breathing rate and depth in coordinated during exercise .

75 / 270
Tidal volume : is the volume of air that enters and leaves the lung in normal one breath ( VT)

Inspiratory reserve volume ( IRV) : is the volume of air that you can take in above the normal inspired tidal
volume

Expiratory reserve volume ( ERV) : is the volume of air that you can force out above the normal expired tidal
volume .

Residual volume : the volume of air remaining in the lungs after you have forcefully exhaled .( RV)

Vital capacity : is the maximum volume of air. Which you can breath out by breathing out as hard
as you can and then breathing in as deeply as possible

Total lung capacity : the sum of the vital capacity and the residual volume
Inspiratory capacity : is the volume of air that can be inspired from the end of normal expiration.

76 / 270
Check list
1. Explain the function of tendons and ligaments
2. Explain how muscles work to straighten leg / bend leg
3. Explain how muscles work to straighten ur arm at the elbow / bend with an angle at the joint
4. Explain whats meant extensors and flexor
5. Describe the structure of muscle fibres
6. Explain the importance of myoglobin
7. Compare and contract between fast twitch fibres and slow twitch fibres
8. Explain why fast twitch muscle fibres fatigue rapidly occurs ?

9. Explian how the cardiac cycle and sequence of muscular contraction in heart is coordinated .
10. Explain the role of SAN
11. Explain the role of AVN
12. Describe what’s an ECG.
13. Label the waves on the ECG
14. Define homeostasis .
15. Describe the feed back mechanism
16 name and describe a positive feed back mechanism
17. Describe the changes in heart that cause an increase in cardiac out put .
18. Describe how the changes in heart rate is coordinated / stimulated as the person exercise
active level increases . 77 / 270
19. State the role of chemoreceptors in stimulating heart rate
20. What stimulates the increase in heart rate during exercise
21. How increase heart rate is stimulated
22. State two other factors stimulating change in heart rate
23. Explain the role of baroreceptors during exercise .
24. Define
Tidal ( VT)
Residual
Expiratory reserve volume (ERV)
Inspiratory reserve volume ( IRV)

Vital capacity
Total lung capacity
Inspiratory capacity

25. Identify each on trace of spirometer

26. Describe how breathing rate is maintained
27. How increase in breathing rate and depth in coordinated during exercise .

78 / 270
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ab
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Dr

D r. Nihal G abr 117 79 / 270

 :
r
ab
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Dr

D r. Nihal G abr 118 80 / 270

 r
ab
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D r. Nihal G abr
((6.26) 119
9 -
1843 - 83
81 / 270
Individual 1 non of the treatments stimulated normal oxygen consumption
Individual 2 : all three treatments stimulated normal oxygen consumption
Individual 3 : only succinate and TMPD stimulated normal oxygen consumption
individual 4 : only reduced TMPD stimulated normal oxygen consumption

r
Puruvate and malate treatment are needed to act on complex I

ab
Succinate treatment acts on complex II
Reduced TMPD treatment acts on cytochrome C
lG
Individual 1 defects is in or after cytochrome C ..evidence that non of the
treatments to any of the ETC shown an improvement in oxygen consumption .
ha
Individual 2 defect is in before complex I ….evidence that the oxygen consumption
was improved back to normal , after any of the treatments.
.Ni

Individual 3 defect is in complex I …. evidence that the oxygen consumption was

Dr

improved back to normal , after succinate treatments .

Individual 4 defect is in complex I ,II and III…. evidence the oxygen consumption
was improved back to normal , that after reduced TMPD treatments

D r. Nihal G abr 120 82 / 270

 r
ab
lG
ha
.Ni

X
Dr

Tendons

Thinking
When one muscle contract the other relax
Where muscles can pull but never push
Muscles can either be extensor or flexor but not both
Antagonistic muscles allow the control of movement .

D r. Nihal G abr
83 / 270
 Actin

Z line

r
ab
Myosin
M line
lG
ha
X
.Ni
Dr

X
X
X

D r. Nihal G abr
84 / 270
 Repeated
Direct
Binds to troponin
Change in shape of troponin
Causing the movement of tropomyosin
Exposing myosin binding site on the actin filament
Allow myosin head to bind to actin and form actin myosin bridge

r
ab
lG
ha
.Ni

Attaches muscle to a bone

Dr

Being non elastic

So it transfers the force (pull action ) of muscle which contracts to
move the bone

D r. Nihal G abr
85 / 270
 r
ab
lG
ha
Skills
.Ni
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As the ADP increases , the activity of the isocitrate dehydrogenase

increase .

Reduced NAD , decrease the activity of isocitrate dehydrogenase

D r. Nihal G abr
86 / 270
 Measuring breathing volume using spirometer

Counterpoised by weight to facilitate the

upward movement .

Nose clip to ensure all

breathing occurs
through mouth from air
inside the chamber of
spirometer

Spirometer has a closed chamber filled with air attached to a movable pen which draws the
trace on a graph paper on a rotating drum .
When the person breaths in , the lid is pulled / move down wards
When the person breaths out , the lid is pulled upwards .
87 / 270
88 / 270
 Step 1 is calibration
Volume
Part 1: Calibration
The spirometer must be calibrated before use, to allow quantitative readings to
be taken.
To calibrate the vertical scale ( y axis )
1. Completely empty the spirometer of air. Allow the pen to touch the trace
paper and make a mark.( mark the initial position of pen ) Time
2. Add 1 dm3 of air to the spirometer and mark the paper again .
3. Use these marks to calculate how many squares on the paper are equal to 1
dm3. Calibrate the spirometer for volume on y axis ( / dm3)

To calibrate for the horizontal ( x axis )

The horizontal scale is much simpler to calibrate as the kymograph will have a
speed setting controlled by a dial. Make a note of the speed setting on the
trace paper, for example 0.5 mm per second ( adjust the rotating speed of
kymograph at 1 or 0.5 mm/ s) '

iii. 1.§
Calibrate the spirometer for time on x axis ( / seconds to )
ñ¥*÷÷
h%%
89 / 270
Step 2 procedure Reading

1. A member of staff will fill the spirometer with oxygen from a compressed gas cylinder.
2. Attach a disinfected mouthpiece to the tube. Switch the spirometer to the open or ‘air’ position.
3. Instruct the subject to place a nose clip on their nose and then place the mouthpiece in their
mouth. They should breathe normally for a few minutes, to become comfortable with the apparatus (see
figure A).
4. Turn on the kymograph so it begins to rotate. After the subject exhales, move the spirometer switch to
the on or ‘chamber’ position so they are able to take a full breath from the chamber.
5. The subject should continue to breathe normally for 30 seconds.
6. Switch the spirometer back to the ‘air’ position and instruct the subject to remove the
mouthpiece from their mouth. Switch off the kymograph.
7. Return the spirometer to the ‘chamber’ position and purge the chamber by lifting the floating part up
and allowing it to drop a few times. The spirometer is now ready to be refilled with oxygen.
8. Once the spirometer has been refilled with oxygen, keep the switch set to the air position.
9. Ask the subject to exercise for 60 seconds (star jumps are a good exercise).
10. Switch on the kymograph so it begins to rotate again. After completing the exercise, the subject
should put in the mouthpiece. Immediately switch the spirometer to the ‘chamber’ position. Allow the
subject to breathe for approximately 30 seconds, then switch the spirometer back to the ‘air’ position.
Note that you may be provided with spirometer traces to interpret rather than carrying out the procedure
yourself.

90 / 270
 Step 3 analysis to spirometer trace

Tidal volume : is the volume of air that enters and leaves the lung '

in normal one breath ( VT) etrde

'

innate
equal the height from peak to trough of a single breath ( dm3)

Inspiratory reserve volume ( IRV) : is the volume of air that you

IRV > ERV
can take in above the normal inspired tidal volume …dm3

Expiratory reserve volume ( ERV) : is the volume of air that you

can force out above the normal expired tidal volume …dm3

Residual volume : the volume of air remaining in the lungs after

you have forcefully exhaled .( RV) ..to prevent alveolar collapse
…dm3

Vital capacity : is the maximum volume of air. Which you can breath out by breathing out as hard as you can and
then breathing in as deeply as possible ( VT + IRV+ ERV) =. dm3
difference between peak and trough for deep breath on spirometer trace
Breathing rate : number of breath in 1 minute ( bpm)
Record the time for the trace then divide number of peaks by time taken / count number of peaks per min
Minute volume = breathing rate x tidal volume …( total volume of air entering or leaving the lung per min…dm3/min
91 / 270
Questions and answers

Plan an investigation In general

Independent variable. ( values + units )

Controlled variables ( 3 abiotic + 1 biotic ) ……..age / gender / BMI / state of health / smoker or
non
(Methodologies )Number of participants / samples….
How these variables are controlled if possible

oÉ Time interval
Control experiment …without factor under investigation for comparison
Dependent …..measure vital capacity …..calibration …how to measure VC
Repeat ….( repetition for each conc / level of exercise )
Larger number of people / sample for each independent variable

1. Allow calibration of spirometer

Calibrate the spirometer for volume on y axis
Calibrate the spirometer for time on x axis

2. Controlled variables
Males and females of Same age , same health state , same being non smokers ….biotic
External temperature should be kept constant using an air conditioner
92 / 270
3. Allow the participants to rest for 5 mins , then start breathing through the mouth piece of spirometer( while
nose is being clipped )
4. Use the spirometer trace to measure …….
A) tidal volume ; height from peak to trough of one breath ( dm3)
Where one peak is equal to one breath
B) breathing rate : by counting the number of peaks on minute ( or every 15 seconds then multiply by 4) to get
the breathing rate in bpm
C)minute volume ; tidal volume X breathing rate
D) amount of oxygen consumed / absorbed ( rate of oxygen absorption ) :

The amount of oxygen consumed is found by comparing / difference the lowest point of a trace at the start of a time period
with the lowest point of the same trace at the end of this period( difference between first and last peaks in one minute.)

5. Repeat 5 more times for each person and calculate

average ( VT / B.R / minute volume /….) for both
males and females
And compare

93 / 270
1. Suggest why soda lime was placed in the spirometer.
2. Describe two ways in which the spirometer trace would look different if the subject had
been exercising more vigorously during the investigation.
3. During the investigation, the oxygen consumption is greater after exercise then before. Suggest a reason
for this difference.
4. State how the waves for the subject would change if the rate at which the kymograph rotated was
increased.
5. Design an investigation using a spirometer to investigate the effects on tidal volume of a subject holding
their breath.
6. Suggest one reason why it was necessary to select only heathy students for this investigation.+ safety
needed to be taken into account ..( risk of injury / infection from mouth piece / exposure to soda lime )
….ethical concerns …( volunterres told about any risk / particpants with any health issue shpuldnt be
taken)

Answers in next page

94 / 270
 1. Role of soda lime

Soda lime absorb CO2

1. Safety ; Soda lime prevents dangerous build up of Co2 in the chamber to a toxic level
2. Allow oxygen consumption to be measured :
Exhaled Co2 is equal to consumed oxygen
Co2 removed by soda lime .
So total volume inside closed chamber of spirometer decrease so allow inclination of the trace

2. Shape of trace if exercising

Longer peaks ( peaks are higher )and troughs would be lower

more peaks = Waves would be closer together
The size of the wave / amplitude of the wave will be higher

3. Reason for increase in oxygen consumption

Aerobic respiration requires oxygen to produce energy.

• Exercise requires more aerobic respiration for the extra muscle contractions.
Mention lactic acid and anaerobic respiration as well .

4. State how the waves for the subject would change if the rate at which the kymograph rotated
was increased.

They would be further apart

95 / 270
6. Suggest one reason why it was necessary to select only heathy students
for this investigation

• Risk of infection of communicable diseases (for example, a named disease).

• Infection of the lungs impairs lung function.
• There is a risk to unhealthy/unwell students undertaking exercise…
So safety concerns
Risk of damage to muscles / ligament’s / injury / joints
Exposure to soda lime / infection from the mouth piece

Also so ethical concerns

Volunteers should know about any risk
Any participant with health issue Shouldn’t be taken

96 / 270
 Exam-style questions
1. Figure 1 shows the spirometer trace of a student while at rest for 2 minutes.
The student breathed in and out normally for the first minute then took a deep breath in
and immediately breathed out as much as possible.

(a) A (1)
4 1 (b) C (1)
3.6
(c) D (1)
.

(d) 1 L OR 1 dm3 (1)

Figure 1

(a) Identify the letter, in Figure 1, which shows the vital capacity of the student.
(1)
(b) Identify the letter, in Figure 1, which shows the inspiratory reserve volume of the
student.
(1)
(c) Identify the letter, in Figure 1, which shows the total lung volume of the student.
(1)
(d)
(1)
(e) What is the breathing rate of this student during the first minute?
(1)
(f) Using information from Figure 1, calculate the respiratory minute ventilation for this
student during the first minute. Show your working.
(2)
(g) The student had a mass for 70 kg.
Using information form Figure 1, calculate the rate of oxygen consumption for this
student during the first minute, in litres oxygen per kg body mass per second. Show
your working.
4-3.6=0.4/70= (3)
(h) While still connected to the spirometer, the student cycled on an exercise bike for a
further 2 minutes.
On Figure 2, sketch the spirometer trace for this student as they cycled. Start your
trace at the positioned on the y-axis.
(3)
Answers
in next
page
© Pearson Education Ltd 2019. Copying permitted for purchasing institution only. This material is not copyright free.
Practical activities have been safety checked but not trialled. Users may need to adapt the risk assessment
information to local circumstances. This document may have been altered from the original. 1
97 / 270
 Answers

(a) A (1)
(b) C (1)
(c) D (1)
(d) 1 L OR 1 dm3 (1)
(e) 12 breaths per minute (1)
(f) 12×0.5(1)=6Lminute−1 (1)
Correct answer with not working gets 2 marks
(g) 0.4 L used in one minute (1)
0.4/60 = 0.0067 Litres per second (1)
0.0067/70 = 0.000095 L kg−1 s−1 or 9.5 × 10−5 L kg−1 s−1 (1) Correct answer
with no working gets 3 marks

98 / 270
 Topic 7C
Control of the internal
environment
A2 Biology Edexcel
WBI15 unit 5

Dr. Nihal Gabr

99 / 270
11/ 2/2023
Part 1
Control of body temperature
Signaling pathway ( TF)

100 / 270
Control the temperature by negative feed back mechanism: Thermoreceptors in skin
detect change in temp
Negative feed back mechanism :
1. Changes in the factor away from set point act as a stimulus
Thermoreceptors in
2. Detected by receptors hypothalamus detects change
3. Causing a release ( from central control) of hormone or nerve impulse sent
in blood temperature / core
4. To reach to target organ ( effector )
5. Effector will perform a correction action temp
6. Factor returns to norm /set point

1, change in temperature away from the norm / set point act as a stimulus.
2. Detected by the THERMORECEPTORS in the skin .
Detected by thermoreceptors in the hypothalamus
Mention an example
3. Thermoreceptors send impulses to the hypothalamus
( sweat glands )
Hypothalamus ( central control) act as a thermoregulatory center
4. Brain / hypothalamus send nerve impulses to effector
5. Effector carry a response ( correction action)
6. Blood temperature falls / increase and return back to the normal / set
point / norm ….so impulses from thermoregulatory center cease .( stop)
7. By homeostasis

101 / 270
 ☀
In case of increase in core body In case of decrease in core body
temperature or temperature temperature or temperature
receptors in skin detects an increase receptors in skin detects a decrease
in the temperature of the in the temperature of the
surroundings. surroundings.

1, vasodilation …
Arterioles in skin gets wider [Link]:
Arterioles in skin gets narrower
So more blood flow in capillaries near the skin surface
So less blood flow in capillaries near the skin surface
So more heat lost to surroundings
So less heat lost to surroundings
2. Increasing sweat production Or shunt dilate so less blood flow to skin
So more heat loss by water evaporation from
2. Decreasing sweat production
skin surface using excess latent heat .
So reduce heat loss by reducing water evaporation from
skin surface
3. Hair erector muscle relaxes , so they lie flat
reducing layer of insulation., and allow more 3. Hair erector muscle contraction , so trap layer of warm
evaporation air ( good insulator)

[Link] adrenalin production [Link] in adrenalin production

Increase in metabolism / respiration so more heat
Decrease in metabolism / respiration so less
generated
heat generated
+ increase in salivation / panting
5. shivering involving skeletal muscle contraction..so heat
5. Inhibition of shivering so less heat generated generated and absorbed by blood
102 / 270
Panting help stabilise body temperature of animals :

Panting causes heat loss

Because water evaporated from mouth
Using heat energy from blood
Panting increases air movement over the tongue / through the mouth
Where increase in air movement increase in rate of evaporation

Panting generates small amount of

heat , suggest why?

Panting involves muscle contraction

Muscle contraction requires energy from respiration
Where respiration releases heat energy

103 / 270
Endocrine vs nervous system

Impulses

Slower
& Faster

104 / 270
Some hormones are released

Many hormones are released in response to other hormones or chemicals in blood

Example pituitary gland in brain

Chemicals like change in blood glucose concentration ..controlled by a negative feed back loop

Over all what controls a

release of a hormone can be
1, nervous system
2. Other hormones
3. Chemical substances

105 / 270
Read

-
X.

106 / 270
 Transcription factors

Transcription factors are proteins acting as chemical messenger involved in the process of
transcription of DNA into a mRNA …….which is followed by translation for protein synthesis

Promoter Gene
Enhancer

RNA polymerase
m mRNA
Transcribed

TF Can form part of protein complex , bind to the DNA -at the promoter ….that enables the RNA polymerase to
bind to DNA at the promoter and
A) transcription of gene is initiated on DNA to mRNA ( activator ) / gene is switched on.
B) transcription is prevented ( repressor) / gene switched off .

TF = activator
proteins

TF= repressor
proteins

107 / 270
TF is to regulate ( turn on and off) the genes in order that they
expressed in the right time and in the right cell and in the right
amount through out life time .

Allow response to environmental stimuli , such as switching on

the correct genes to respond to high environmental temp.
As correct genes expressed in response to very high
temperature .

Different types of hormones act as DNA transcription factors in different ways ….and this how they make
changes in the body
There are two main ways in which hormones can have their effect :
A) the release a second messenger …..( protein / peptide hormones )
B) the hormone enter the cell ….(steroid hormones )
Hormones Stimulate cell signaling cascade
Act as signaling molecules

Peptide hormones ( hydrophilic)

Steroidal hormone ( hydrophobic)
iz
↑
cocoedatwa 108 / 270
 Peptide hormone Adrenaline
1
1. Peptide hormone ( ….) bind to specific receptor on the cell

⑧ ·
surface membrane .
2, cause conformational change in the shape of receptors
3. This will cause the beginning of a serious of membrane
bound reactions
4. Resulting in the formation of a second messenger inside the
cell as Cyclic AMP .
G protein
Receptor has a
2
A) . The second messenger then activates a number of different complemnatry shape to
3 Activate the G protein 4
the adrenaline
enzymes with a cell within a cell altering metabolism . Which will activate ATP
the adenylate
Such as increase cellular respiration , muscle contraction , Conformational change in The activated enzyme

shape of receptor
cyclase ( membrane catalyse the conversion
relaxation of smooth muscles in blood vessels , protein ). of ATP into Cyclic
AMP ( the second
messenger).

B) the second messenger Cyclic AMP bind to other chemicals cyclic AMP
which pass into the nucleus and act as DNA transcription

⑳
transcription- A
factors B
factors
activation. Activate a
TF bind to promoter region of a certain gene TF number of
This activates the promoter region which switch on the gene by different
allowing RNA polymerase to bind Allow gene expression enzymes ,alter
RNA transcription is initiated producing mRNA which is then cell metabolism
translated into a protein 109 / 270
 Steroid hormones

1. Such as oestrogen and testosterone are lipid soluble

Can pass through phospholipid bilayer
And act as an internal messenger them selves .

2. Hormone bind to receptors inside the cell

3. And form hormone receptor complex passes through pores in the

nuclear membrane into nucleus

4. Hormone receptor complex ( hormone attached to receptor ) act as

TF
Regulating gene expression and switching sections of DNA on or off

Where they( hormone receptor complex / TF ) bind to the promoter

region which can swutch on the gene by allowing RNA polymerase to
bind to promoter ………transcribed into mRNA …then tarsnlated into
protein

TF can switch off the gene TF = transcription factor

110 / 270
21/2/2023
Practice on 7B and 7C

Dr. Nihal Gabr

111 / 270
 Refe
internet. Direct

Maintenance of the physiological conditions inside the body at near constant

level despite the changes in the environment and in then body ….by negative feed
back mechanism)

r
ab
lG
ha
.Ni
Dr

D r. Nihal G abr
112 / 270
 Linked to AS

Break down of 1, 4 and 1, 6 glucosidic bonds

Between alpha glucose
Using water

r
ab
Skills
During exercise , there is an increase in energy demand
lG
Means muscles need more ATP for more muscle contraction
During exercise there is more sweat to allow cooling down of the body where water
evaporates using excess heat energy from the blood
ha
Adrenaline stimulating glycolysis so more ATP is produced
ACTH …stimulate the increase in glucose concentration to be sent to the blood as
.Ni

respiratory substrate.
Glucagon will stimulate the break down of glycogen to increase glucose
concentration in blood .
Dr

Insulin , ensuring maintaining the norm value of the glucose concentration in blood
Aldosterone , ensure reabsorption of sodium ions to replace lost salts in sweat
ADH , more water reabsorbed back into blood to replace / compensate the lose
of water in sweat

D r. Nihal G abr
113 / 270
Some of Hormones are proteins
So transcription factorS are proteins that binds to promoter regions on
the DNA
Where TFSare needed to control the switching on of some genes such as
gene coding for glucagon so it can be synthesised
By allowing RNA polymerase to bind to promoter to initiate transcription
of gene

r
Producing a mRNA Linked to AS unit

ab
To be translated into proteins ( these hormones) . 2
Gene regulation
lG
Or TF can switch off the gene
To stop the synthesis of some hormones like insulin
ha
TF……………….level of production of some hormones
.Ni

Protein
mRNA
Dr

Proteins
Bind to promoter
Allow RNA polymerase bind to promoter
Initiate transcription
mRNA
Translated into a hormone ( protein ) …glucagon / ACTH / adrenaline

Or TF can switch off the genes to stop the synthesis of some hormones like
D r. Nihal G abr
insulin
114 / 270
 O2

Gene
Code
EPO

r
ab
lG
The lower the concentration of the oxygen , the more the EPO Skills
ha
synthesised .
As time increase ( increase in umber of hours ) , the more the
EPO synthesised at (all oxygen concentrations ) .
.Ni
Dr

D r. Nihal G abr
115 / 270
 Signalling Molecul

I
Low oxygen concentration stimulate the production of cyclic AMP
acting as a second messenger
This allows the activation of transcription factors

I Transcription factors bind to promoter region of EPO gene

Allow RNA polymerase to bind to promoter region
Increasing rate of transcription of EPO gene

r
So EPO production / synthesis increase

ab
lG
ha
ci
E x7
.Ni

printt
Dr

-0
-
-
W

D r. Nihal G abr
116 / 270
 Skills

red blood cells will transport oxygen

r
Yet in the fast twitch fibres there are fewer mitochondria

ab
So any additional oxygen will have a limited additional effect
Also fewer capillaries in fast twitch muscle so poor blood supply so little extra
oxygen is received
lG
So in fast twitch respiration is mainly / primarily anaerobic
Short time duration of race means , so no need for extra oxygen .
ha
.Ni
Dr

Not being fair

Repeated
Unethical
Direct
Health risks to athletes ( raised blood clotting risk )
Cost to-medical services Of health implications

D r. Nihal G abr 133 117 / 270

 4.
-
0

r
ab
0 lG
ha
.Ni

X
Dr

D r. Nihal G abr 181 118 / 270

 /=
X

r
ab
X
4 -1 = 3 dm3
3 / 6 = 0.5
lG
ha
.Ni
Dr

D r. Nihal G abr 182 119 / 270

 r
ab
lG
ha
.Ni
Dr

450 cm3 ……..0.45 dm3

18 x 0.45= 8.1 dm3 / min

D r. Nihal G abr 183 120 / 270

......

-
Recording total time taken by then spirometer to draw ' the trace
Count of peaks on trace are counted
Divide the number of peaks by time

r
ab
lG
ha
.Ni
Dr

As the cyclic speed increase , the tidal volume increase

Increasing the cyclic speed by 25 km / hr , the tidal volume
increased by 2400 cm3.
Steepest increase was observed by increasing speed from 0 to 10
km / hour where it showed an increase by 1100 cm3

D r. Nihal G abr 184 121 / 270

 Direct

r
ab
lG
ha
.Ni
Dr

Signaling cascade
Enzyme 1
Enzyme 2
Enzyme 3

D r. Nihal G abr 185 122 / 270

 r
ab
lG
ha
.Ni

Skills As the age increases , the median FEV1 decrease

Dr

The lower the altitude , the lower the median FEV1

D r. Nihal G abr 186 123 / 270

 Skills

Exhalation
Decrease in the elasticity of the alveolus walls
The intercostal muscles and diaphragm become weaker
Alveoli number
Fewer number of alveoli due to a disease such as emphysema
Elasticity of alveolus wall
Intercostal muscles and diaphragm
Smoking …lung cancer /
emphyseae
High altitude

r
Lower O2 in inhaled

ab
Skills
Low altitude

Less O2 concentration in the atmospheric air at high altitude

lG
So he must inhale deeply and forcefully
To take in more oxygen ( larger vital capacity )
As he had stronger diaphragm and intercostal muscles
ha
.Ni

⑧
Less O2 concentration in the atmospheric air at high altitude
Dr

So he must inhale deeply and forcefully

So mor air need to be exhaled / breathed out

D r. Nihal G abr 187 124 / 270

 Skills

Collect data from one group of andean men and from the group of
North America men .

Where for each individual in each group measure the volume of the
air in each breath using spirometer

r
Then divide by time taken to calculate the rate of breathing per

ab
min

lG
For each group , find the median .
ha
.Ni
Dr

D r. Nihal G abr 188 125 / 270

25/2/2023
Part 3
Excretion

126 / 270
Excretion Its the removal of toxic substance , waste products of metabolic reactions
As well as removal substances found in excess out of the body

Deamination

Break down of excess amino acids in liver , to remove amine group ( NH2) …forming ammonia
…….which is toxic ….so ammonia combine with CO2 in urea cycle ….form urea

This because amino acids cant be stored as they are alkaline due to their amine group so if stored
they would increase pH to a dangerous level

"
H
2 H
N C C- OH O2
20
NH (C C- OH

R R

Keto acid …to kreb’s Cycle

Ammonia is highly toxic so converted into A) respired to produce ATP
urea by adding CO2 using ATP in urea B) or converted into glucose
cycle .
2 NH3 + CO2 ………………CO ( NH2)2 + H2O

Urea Water
In ornithine cycle
127 / 270
The ornithine cycle
2NH3 + CO2…………CO ( NH2) 2 + H2O
Urea + water

They cycle has 3 intermediate molecules :

Ornithine , citrulline , and Arginine

Ornithine ,urea
Ammonia
Co2
Water
Water

Citrulline Arginine

Ammonia Water

128 / 270
Structure of the kidney

From any mechanical force

Glomerulus PCT

Bowman’s capsule
Loop of henle
Blood supply Collecting
duct
The kidney is supplied with blood from renal artery
Where the renal artery is a branch from AORTA , which takes blood away from the heart under high pressure
The blood leaves the kidney through renal vein

Epithelium
Layer of cells lining an organ
Squamous
Cuboidal Columnar

-
Jen
Ciliated
129 / 270
 PCT ⑧
Walls are lined with cuboidal epithelial cells with MANY DCT
MICROVILLI Walls formed of cuboidal
Renal capsule
epithelium with no microvilli
Closed end , cup
shaped with
glomerulus where
filtrate is collected …..
Lined by squamous
epithelium Collecting duct
Wider tubules
Walls lined with
Cuboidal epithelium
without microvilli
Glomerulus
Becomes increasingly
A bundle of capillaries …with wide as it empties its
smooth endothelium content in to the pelvis
( squamous ) and pores and Loop of henle
surrounding the capillaries
there is a basement membrane Long hair pin that extends from the cortex down to the medulla
and podocytes. and back again
Thin section are formed with squamous epithelium , thick section
are formed of thicker cuboidal cells with no microvilli 130 / 270
Squamous epithelial cells
1. Glomerulus
2. Bowman’s capsule
3. Thin section ( descending limb )

Cuboidal epithelial cells

1. PCT with microvilli
2. Thick section ( ascending limb ) without microvilli
3. DCT ( without microvilli )
4. Collecting duct ( without microvilli )

Wi Bloodin glumaln
2.
water Minal salts glue anis ac

amosig pleana Peter RR Wis. Plat.

SPressu
wi Burn's cap.
sane.
X xx
x

131 / 270
A Ultra filtration

1. The blood coming in the afferent arteriole Under high

pressure, the efferent arteriole has a smaller diameter than
afferent arteriole , build up a pressure in the glomerulus
….forcing fluid out of the glomerulus through capillary
pores ( FENESTRATIONS IN THE capillary endothelium)
into Bowman’s capsule .

Afferent arteriole -..

Efferent arteriole
Fenestrations of
↑

glomerulus

What resist the movement of filtrate intonbowman’s

2. Basement membrane made of collagen and capsule?
glycoproteins , that act like a mesh and a selective barrier … 1, capillary endothelium
allow water and ions ( small molecules) to pass through but 2, basement membrane
large molecules don’t pass like RBCs , WBCs , large plasma 3. Epithelial cells of capsule / podocytes
4. The lower water potential of blood in glomerulus ..creat
proteins .
osmotic pressure opposing to the hydrostatic pressure .

3. Podocytes , cells with projections that don;t form a

complete lining around the capillaries …..the foot like Solution :
extensions form gaps known as SLIT PORES …molecules 1. Endothelium of glomerulus capillaries have pores ( fenestrations)
[Link] allow the filtrate to pass through slit pores
will pass through slit pores into BOWMAN”S capsule
3. Hydrostatic pressure > osmotic pressure . 132 / 270
Blood renal barrier ?

1, capillary endothelium
Which has FENESTRATIONS to increase pressure

2, basement membrane
made of collagen and glycoproteins , that act like a mesh and a selective barrier …allow water and
ions ( small molecules) to pass through but large molecules don’t pass like RBCs , WBCs , large
plasma proteins .

3. Epithelial cells of capsule / podocytes

cells with projections that don;t form a complete lining around the capillaries …..the foot like
extensions form gaps known as SLIT PORES …molecules will pass through slit pores into
BOWMAN”S capsule
They also maintain the basement membrane in position .

Capillary wall / endothelium

Basement membrane

Podocytes

133 / 270
 .
Basement membrane
Endothelium
Mitochondrion
of capillary

Proximal
tubule lumen

Blood Tight junctions

Plasma Blood

Basal side Apical side

( facing ( facing lumen)
capillaries
PCT

The PCT is tangled to increase surface area for absorptions

Lined with cuboidal epithelium with microvilli and many mitochondria

1. Microvilli : increase surface area for absorption of sodium ions and glucose …they carry more co transporters
for faster rate of absorption.
2. Many mitochondria : to produce ATP for active transport of sodium ions out of cells
3. Tight junctions : formed between adjacent cells so that fluid can’t pass between cells
4. Folded basal membrane ; with many transport proteins ( sodium pump )
5. Aquaporins : channel proteins for water movement by osmosis
6. More RER for increased protein synthesis .
134 / 270
for
Blood

i t he
Cell membrane Pump

Filtrate ( PCT lumIen )

135 / 270
 ...
Proximal
tubule lumen
'

Na+
Blood Facilitated diffusion

Plasma K+ Glucose
Glucose Co transported by
secondary active
transport

Most of the filtrate is reabsorbed in PCT

Where the membrane lining the lumen of PCT has microvilli to provide larger surface area for absorption .
1. SODIUM POTASSIUM PUMP
In the lateral and basal membrane ..where sodium pumped out of the cells into blood
Against the concentration gradient
Using ATP from respiration in mitochondria
Thus decreasing sodium ion concentration inside the cells .
2. So sodium ions will diffuse into epithelial cells from the fluid in lumen of PCT ( filtrate ) ..by facilitated diffusion…
where sodium ions co transport glucose and amino acids , where glucose and amino acids enter the cell by
secondary active transport …..which in turn diffuse out of epithelial cells into blood by facilitated diffusion ..so. most
glucose , amino acids , chloride ions are reabsorbed as well as water 136 / 270
Notice
Secondary active transport means its doesn’t use ATP but occurs secondary to active transport of sodium ions by
sodium pumps in the basal side ..

3. REABSORPTION OF WATER :
Where the co transport of solutes into the cytoplasm of epithelial cells ……increase concentration of the
cytoplasm so water moves by osmosis down water potential gradient from filtrate in the PCT lumen into the
epithelial cell cytoplasm through the epithelial cell membrane . …..which in turn enters the blood by osmosis .

137 / 270
28/2/2023
Part 4

138 / 270
 Loop of Henle

Hair pin loop starts at the cortex and extending /descending deep in the medulla of the kidney …..its
role is to provide a concentrated tissue fluid / interstitial fluid in the medulla ……..i.e around collecting
duct…..for water reabsorption from urine in Collecting and DCT into blood in capillaries .

Adapted

Descending loop Ascending loop

1. Descending limb , which is narrow with thin walls that are highly permeable to water
2. Ascending limb , which after short distance is wider with thicker walls that are
impermeable to water and contain protein pumps for pumping ions out .

1. Outside the loop of Henle is the interstitial fluid

2. Over all , as the filtrate moves down the descending limb and up the
amni
ascending limb …………its gets more concentrated first then less pump
concentrated
3. Filtrate that pass from end of the loop to DCT is less concentrated
…….than what enters the loop from PCT as most ion have pumped out .
E.
dffeit

139 / 270
 1. Sodium ions pumped out of the
walls of the ascending limb into
the interstitial fluid.
Increasing solute
2. Lowering water potential of the
concentration Nat
Nat
Cortex 6 Cl interstitial fluid ( medulla ) .
( i.e increasing Salt 3. water will diffuse out of the thin
-

3οο
the concentrationMedulla 400 3 E2
500
descending limb into interstitial
of tissue fluid 600 Saltier fluid by osmosis .
800
4. So the concentration in the lumen
1000
4
1200 NNSaltiest of the descending limb becomes
[Link] moves out of the collecting duct by significantly increasing ( at the tip
osmosis until w.p in urine is equal to the of the pin ) .
water potential of the interstitial fluid 5. At the base of the ascending limb,
….controlled by ADH ….( which sodium and chloride ions will
concentrates the urine. diffuse out of the filtrate …filtrate
will develop progressively higher
8. Counter current multiplier …
water potential .
ensures the presence of water
6. Water potential gradient is
potential gradient drawing water out created in the interstitial fluid
of the tubules into blood . between the cortex and
Fluid is moving in opposite direction in the two limbs of loop of Henle
medulla ..with increasingly lower
Multiplier ….this movement of the fluid in the limbs will cause an increase in the ion
water potential the-further in
concentration of the interstitial fluid in medulla
medulla
140 / 270
141 / 270
Notice the ability of some small mammals,such as rodents, to produce a very concentrated urine is
related to the relative thickness of the medulla in their kidneys.

The maximum concentration of urine that we can produce is four times that of our blood plasma.

Desert rodents, such as gerbils and kangaroo rats, can produce a urine that is about 20 times the
concentration of their blood plasma.

This is possible because

1. the medulla is relatively large
2. and the cells that line the ascending limb of their loops have deep in folds with many Na+–K+ pumps
and
3. cytoplasm filled with many mitochondria, each with many cristae that allow the production of much
ATP to provide the energy for the pumping of sodium ions into the tissue fluid.

4. Longer loop of henle

7
Allowing a greater counter current multiplier effect
So higher concentration od solute / sodium chloride at base of medulla Help them survive desert
So greater amount of water to be reabsorbed from collecting duct

142 / 270
4/3/2023
Part 5
ADH

143 / 270
Control of water in blood

ADH …osmoregulation
Produced in hypothalamus …….secreted from pituitary gland ….blood to target collecting duct
and DCT

ADH made by neuro secretory cells which are specialised

nerve cells , having their cell bodies in the hypothalamus ..and
their axon descending into the posterior pituitary gland ..The
nerve cells transport the hormone down their nerve fibres
(axons) to the posterior pituitary gland where the hormone is
released into the bloodstream.

144 / 270
 A
Decrease in water
potential of blood

Less water in blood

1. Low water potential of blood
Osmoreceptors Baroreceptos

2. Detected by osmoreceptors in the hypothalamus … 2. So blood volume will decrease

where these receptors shrink where water is lost from 3. So pressure of blood on baroreceptors will
these osmoreceoptors by osmosis
decrease , . So baroreceptors wont stretch
3. Osmosreceptors stimulate neurosecretory cells in
the hypothalamus to produce ADH

4. More ADH is released / secreted from the pituitary gland

5. Where the ADH will be carried by blood to the kidney

145 / 270
6. ADH bind to receptors on the cell surface membrane of DCT and
CD …which activate set of enzyme controlled reaction ( activate
phosphorylase enzyme)
7. Leading to movement of ready made vesicles surrounded by a
membrane containing many aquaporins
8. Aquaporins added to the membrane
9. Increasing permeability of CD and DST to water
10. So water will move from filtrate to interstitial fluid ( salty medulla)
to enter the blood by osmosis ….so small volume of urine
( concentrated) increasing W.P of blood back to norm by negative feed
back mechanism

11. Osmoreceptors also send signlas to the thirst center of the brain to
allow you to drink water .

Notice some urea may also move out of cells

through aquaporins ..increasing the conc of
intersitial fluid in the medulla ..so more water
leaves by osmosis .

146 / 270
B
Increased water
potential of blood

More water in blood

1. Higher water potential of blood
Baroreceptos
Osmoreceptors
2. Detected by osmoreceptors in the 2. So blood volume will increase
hypothalamus …where these receptors . So pressure of blood on
swell where more water enters baroreceptors will increase , . So
osmoreceoptors by osmosis baroreceptors stretch .

3. stimulate the pituitary gland to reduce/ inhibit the release of ADH into the blood .
4. Aquaporins will be moved out of the cell surface membrane of DCT and CD back to cytoplasm
as part of vesicles
5. Decreasing the permeability of the membrane of CD to water
[Link] less water is reabsorbed back into blood from filtrate in CD
5. More diluted urine (increase water loss in urine ).
and so reduce volume of blood and the pressure falls again .
6. Water potential of blood return back to norm by negative feed back mechanism 147 / 270
Check list
1. Control the temperature by negative feed back mechanism:
2. Explain how body respond in case of increase in core body temperature or temperature receptors in skin detects
an increase in the temperature of the surroundings.
3. 2. Explain how body respond in case of decrease in core body temperature or temperature receptors in skin
detects a decrease in the temperature of the surroundings.
4. Explain how Panting help stabilise body temperature of animals :
5. Compare between Endocrine vs nervous system .
6. Explain how peptide hormones act as signaling molecules …/ stimulate and trigger transcription of some genes
7. Explain how peptide hormones act as Signaling molecules …/ stimulate and trigger cellular response involving a
change in chemical reactions inside the cell
[Link] how steroidal hormones stimulate and trigger transcription of some genes
9. Define excretion
10. Why amino acids cant be broken
11. Describe deamination
12. Role of ornithine cycle
13. Describe the structure of kidney , nephron
14. Describe ultrafiltration
15. Describe selective reabsorption .
16. Explain adaptation of PCT
17. Explain what are Blood renal barrier ?

148 / 270
Check list
18. Describe how loop of henle is adapted for water reabsorption
[Link] the mechanism counter current multiplication .
20. Explain how concentration of interstitial fluid increase as we move down the medulla …8 steps process
21. Explain how animals living in desert produce more concentrated urine
22. Explain the role of ADH in osmoregulation
23. Explain the role of osmoreceptors and baroreceptors in controlling blood osmolarity

149 / 270
8A the nervous
system and
neurones

Dr. Nihal Gabr

150 / 270
Topic 8A
part 1
Structure of neurones
Spinal reflex
Resting potential

151 / 270
 Structure of nerve cells

Cell body : Contains nucleus , many mitochondria , large amount of RER ….associated for the production of
proteins and neurotransmitters

Dendron Extension from cell body sub divided into dendrites carry nerve impulses towards the cell body

Axon Long fibre carrying nerve impulses away from the cell body

Schwann cells It provides insulation to axon , they wrap themselves around the axon where the
layers of their membranes build up around the axon forming Myelin sheath

The space between adjacent Schwann cells lacking myelin sheath ..( size is around
Nodes of Ranvier
2 -3 um ..occurs every 1-3 mm in neurone of human to enable saltatory conduction
152 / 270
 Sensory
Types of neurones Dendron Longer
Motor end plates
Dendron myelinated
Axon shorter
Cell body towards the middle
No motor end plates

Sensory neurone Relay neurone Motor neurone

Dendron is longer Short dendrites Many Shorter dendrites

Dendron is myelinated X X
Shorter axon Shorter axon Long axon
Myelinated axon X Myelinated axon

Central cell body / towards the middle . . . - Terminal cell body

X X Motor end plates 153 / 270

Types or reflex action

A) according to the synapse

Monosynaptic reflex:
Sensory neurone is directly connected to the motor neurone
Providing a direct communication between sensory and motor neurone ..faster

Polysynaptic reflex : more complex pathways sesnory neurone is connected to one or more relay
neurones which are then connected to motor neurone ..slower

154 / 270
 B) according to the center of reflex
1. Cranial reflex

The brain is the CNS

Center is the unconscious area of the brain
Example : reflex controlling the diameter of pupil …..Pupillary reflex

2. Spinal reflex
The center is the spinal cord ….hand withdrawal / knee jerk

Spinal reflex like hand withdrawal

[Link] …..heat object detected by sensory receptors
2. Receptor ….if temperature receptors detect temperature above the
threshold value…so this will generate an action potential
3. Sensory neurone ..action potential pass along the sensory neuron
to spinal cord
4. Relay neurone ( grey matter of spinal cord ) link the sensory to
motor neurone via the synapse.
5. Motor neurone carry action potential away from spinal cord to the
effector ( biceps muscles of the forearm )
[Link] contract ..bring a response which is raising up the hand away
from hot object
155 / 270
 Resting Types of transporter proteins in the cell surface membrane of axon
Resting
arn
Active movement ( needs ATP )
si
Down
Passive movement ( no ATP )
Sodium potassium pump acts continually to concentration
gradient

D*
Potassium ion protein channels
transport ions ( sodium and potassium across ++ + +
Down
electrical
--

t+ t
membrane ) ..Na +out and potassium +in gradient
-

Down
electrical

mmm gradient

·
A Always open , movement of ions by facilitated
diffusion…allowing movement of potassium ions out
across the membrane down their chemical gradient
a ( i.e concentration gradient) / in down the electrical

. gradient

Action
Voltage gated channels
Proprties of the membrane of axon

8888
1. Axon cell membrane is made of phospholipid bilayer that restrict
Alternate between being
ion movement
open and close …respond to
2. Yet it has sodium potassium pump which act continually to
transport sodium and potassium ions across the membrane ( Na+
the changes in the potential
Out and K+ in difference across the
Potassium VG
3. Has voltage gated sodium and potassium channels , they channels
membrane
alternate between being open and close to allow diffusion of ions Sodium voltage gated channel 156 / 270
 Resting potential

100+
30+ Potential difference = -70 ( less 70 +ve charged ions inside )

Polarised
3 3 6

2 L

3 1. Sodium potassium pump, sodium ions actively transported outside the axon and potassium ion
inside ( using ATP) ..for every 3 Na+ ion pumped out , 2 K+ ions move in ..so becoming more
positive outside ..
2. At rest, We have high K+ ion concentration inside the axon and high Na+ ion concentration
outside axon ( building chemical gradient)
2 membrane is not permeable to sodium ions / eq ;
3. Sodium ion channels are closed so cant diffuse back again into the axon
The membrane of neurone is more permeable to potassium ions so K+ ion will diffuse out of the
axon down its concentration gradient .
4. Making the outside of membrane positive and inside negative … 157 / 270
 5. Electrical gradient will pull potassium back into the nerve cell /axon
Decreasing the positive charge from outside

6Where at -70 mV pd , the two gradients counter current each other (equilibrium is established )and therefore
no net movement of K+ ions …..resting potential

Maintaining pd

Why resting potential requires energy

Sodium potassium pump …..sodium ions are pumped actively out of the axon while potassium ions are actively
pumped inside by sodium potassium pump across membrane.
Against their concentration gradient ….to establish concentration gradient for sodium ions and potassium ions.

Summary for short answered questions

1. Sodium potassium pump,

2. sodium ions actively transported outside the axon and potassium ion inside ( using ATP) ..for every 3 Na+ ion
pumped out , 2 K+ ions move in ..so becoming more positive outside.
Sodium ion channels are closed .
[Link] membrane of neuron is more permeable to potassium ions , through having more potassium ion channels…
K+ ions will diffuse out of axon .
4. So the inside of the membrane is negatively charged compared with outside
5. Maintaining pd 158 / 270
7/ 3/2023
Part 2
Action potential

159 / 270
 Action potential

Threshold potential is the potential difference across the membrane above which an impulse is sent along a
neurone / the point when sufficient sodium ions channels open for rush of sodium ions into the axon

Polarisation….resting potential P.d= -70 mv

Depolarised : changing potential difference -50mv ….+ 40 mv

across the membrane so it becomes less
negatively charged inside ( +ve inside , -ve
outside )

Hyperpolarisation : a decrease in the

potential difference across the membrane
becomong MORE negatively charged
inside Below -70 mV

N
- Polarised

160 / 270
Resting potential A

1. Potassium ion channels are open , voltage gated

potassium and sodium ions are CLOSED

·
I
Depolarisation / action potential
I
Na+ VG open Na+ VG close

2. Stimulus exceeding threshold, increase the permeability of the K+ VG closed K+ VG open

membrane to the sodium ions

Where some of the VOLTAGE gated sodium ions open
Ekt
Resting
Polarise
Therefore sodium ions diffuses into the neurone through the channel down potential

their electrochemical gradient / concentration gradient .

+----

Polarised
E
Being positively charged , this will reverse the potential difference across
the membrane and become DEPOLARISED
3. As more sodium ion diffuse into the neurone / cell , the more volatge
-

gated sodium ion channels open ..greater influx of sodium ions ..positive
feed back mechanism .
Increasing amplitude of depolarisation
4. Once the pd across the membrane reaches +40 mV ..this is known
as action potential

161 / 270
Repolarisation

5. As the action potential reaches +40mv

At this point Voltage gated Na+ ion channels will close
So sodium ions cant continue to enter the neurone

Where some of the potassium K+ VOLTAGE gated channels open

This will cause other K+ VG channels to begin to open
And more K+ outflux down its electrochemical gradient and concentration gradient
Being attracted by negative charge outside of the membrane
So inside of axon will become negative relative to outside .

Hyperpolarisation

The outward movement of K+ ions continue and slight delay of closing K+ VG channels cause a tempeorary
OVERSHOOT of electrical gradient , with axon inside become more negative inside than outside
This nis called HYPERPOLARISATION

Resting potential after hyperpolaristation

7. The voltage gated potassium channels close , sodium potassium pump cause the sodium
ionspumped out and potassium in , where for every 3 Na+ ions pumped out, 2 K+ ions in …
so becoming more positive outside …then electrical gradient will pull the potassium back into
the nerve cell / axon ( postassium ions diffuse back into the axon through potassium
channels ( non gated ) , decreasing the positive charge from outside
restoring the resting potential state of the axon which is now polarised .
162 / 270
 K+ outflux
Na+ VG closed
volded
K+ VG open wel

-t
Na+ VG open
K+ VG closed
Sodium influx
perce

III xt
-> +

Delay in close of VG K+
D
Hyperpolaristaion

Polarised
VG channel closed
Sodium potassium pump + K ( non gated ) channels

Maintain resting potential

163 / 270
-BÑB②B@Mpµ&
Resting potential Polarized (-70mv)

* + + ++

[Link] exceeds the

threshold -50mv
2. Open voltage gated Na+
2
Slight delay in closing of voltage

4 channels .
gated K= ions
-

Na+
¥ '

÷ ÷: :-.
µma:µq-
Na+ open
Influx K+ open . .

Efflux

momma:: ÷ :-.
+

:
K+
Efflux
3
Action potential reaches +40mv inside the axon
…..repolarisation ……voltage gate Na+ close
….potassium voltage gated .channels open
164 / 270
14/3/2023
Part 3
All or nothing
Propagation of nerve impulse
Saltatory conduction

165 / 270
 All or nothing law

1. Nerve impulses are described as all or nothing responses

2. There is a certain level of stimulus , which is the threshold that
triggers the impulse .
3. Potential difference is below the threshold , no impulse
generated / no action potential
And above threshold value , there is an impulse will be generated /
result in an action potential .

4. The action potential is the same regardless of how much the

stimulus is above the threshold value
5. We can determine the size of the stimulus by :
A) frequency of impulses passing in a unit time ….where the larger
the stimulus ,the more the action potentials that are generated per
unit time
B) number of neurones carrying action potential

The threshold has been reached

Resulting in an action potential
Action potentials are all or nothing ( since either they occur
fully or they dont occur at all )
166 / 270
 Second action C
Propagation of nerve impulse
potential is initiated :
A

Resting potential Yet at the site of first

+
High sodium ion action potential …
concentration repolarisation ..K= VG
outside and high channels open and
potassium ion K+ ions move out of
concentration the axon …Na+ VG
inside Repolarisation
closed …followed by
And hyperpolarisation
hyperpolarisatio
B n D
Action potential Third action potential
( depolarisation): initiated..by the second
Na+ VG channels action potential .
open and K+ VG At the site of first
closed , Na+ flow action potential …K+
inside into the diffuse back into axon
j
axon ..depolarizing restore the resting
the membrane potential
Site of second action potential…
repolarisation and
167 / 270
hyperolarisation
 ⑱54.95
Read
Propagation of nerve impulse As one region of the axon produces an
action potential and become
depolarised ,
it acts as a stimulus for the
depolarisation of the next region of the
axon/ membrane . This reversal of
electrical charge is reproduced and
action potentials are generated along
each small region of the axon
membrane .
As one action potential triggers the
next , the previous region of the
membrane returns to its resting
potential i.e its repolarised.
The size of the action potential
remains the same from one end of the
axon to the other .
Strictly speaking , nothing physically
moves from place to place along the
axon of the neurone , but rather the
reversal of electrical charge is
hyperpolarisation reproduced at different points along the
axon membrane .....like MEXICAN
WAVE.

Cant be depolarised
( depolarisation is not possible becasue in repolarisation and
hyperpolarisation state all the sodium voltage gated channels closed

Refractory period ..brief period of time following an action potential. When a neurone can’t be
stimulated ( period of time where sodium gated channels don’t respond to depolarisation)
1) ensure action potential are separated without merging …limiting number of action potentials
passing by action per unit time ….determine frequency of action potential
2) allow the action potential to travel in one direction . As when one part of the neurome membrane
depolarises the previous part is till hperpolarised

168 / 270
 🔒

Na+ ion voltage gated channels

Na+ volatge closed .
gated channels K+ volatge gated open ….till
open overshooting .
K+

Refractory period in english

period during which an organ ,
cell cant repeat a particular
action . …not ready to receive
another stimulus

Refractory period inactivation of voltage gated sodium channels ..which occurs at the peak of action
potential ( +40 mVolts ) …and persist through most of the overshooting period .
Overshooting describe …….
Refractory period ensure that an action potential will only travel forward down the axon not back
wards
Read to understand 169 / 270
How action potential is transmitted along the myelinated neurone

Depolarised
Na+voltage gated
channels open

T
Repolarisation
K+ VG open
Na+ VG closed

170 / 270
How action potential is transmitted along the myelinated neurone

B
A

Depolarised Polarised
Na+voltage gated
channels open Resting potential

A 1. Action potential ( depolarisation) ..Na+ voltage gated channels open

……….sodium influx ….cause depolarisaation at the nodes of RANVIER

B 1. Action potential stimulate the neighbouring area if the membrane

2. Sodium is attracted to area of the resting potential. ..( local circuit) Na+ ….._ve
3. It will stimulate the opening of the volatge gated Na+ ions …( SECOND
DEPOLIRASTION )
Transmission is in one direction due to A Refractory period ( repolarisation and
hyperpolarisation) …..where Na+ VG closed ..( recovering from the action
potential ) at +40 mV and K+ VG open …pottasium efflux and the membrane
becomes replaorised .

171 / 270
4. Where myelin sheath is a part which doesn’t get depolarised as myelin sheath prevent movement of
ions in or out ( electrical insulator preventing leakage of ions )

5. So depolarization happens at the nodes of Ranvier

6. Set a local circuit between depolarised nodes and the successive node
7. Action potential will jump from one node to the other along the myelinated nerve fibre in a process
called SALTATORY Conduction

Factors affecting the transmission of action potential

1. Myelin sheath ( Schwann cells covering the axon ) .

Allow depolarisation ( action potential ) only at nodes of RANVIER where there is no myelin sheath at
nodes
Set a localised circuit between adjacent nodes of Ranvier which occurs over longer distance.
So the action potential will jump from one node to another in a process known as Saltatory conduction .
Allow faster conduction of action potential .

2. Diameter of the axon ( nerve fibre) :

The greater the diameter ( thicker ) of an axon , the faster the speed of transmission !!!! III!!!
….less ions channels responsible for maintaining the resting potential ..so harder to
maintain the resting potential + less resistance
Less leakage of ions ..harder to maintain resting potential
172 / 270
21/3/2023
Part 4
Synapse

173 / 270
Synapse

Synaptic cleft
Synaptic knob ….contain mitochondria , ER , synaptic
vesicles
Receptor molecules found on surface of post
synaptic membrane

Neurotransmitter

chemical neurotransmitters which are needed to

transmit the nerve impulse across the synapse

Released from vesicles in the presynaptic neurone /

knob

Diffuse across the synaptic cleft and bind to receptors

on the post synaptic neurone

Initiating the action potential in the post synaptic

cell / membrane / neurone

174 / 270
 L
1. An impulse arrive at the synaptic
knob

3. Calcium diffuse 2 . Depolarisation reach the

into cytoplasm preseynaptic membrane , the
knob voltage gated Ca+2
channels open .

4. Calcium trigger movement of

vesicles towards the presynaptic
5, fuse , release by exocytosis
membrane

6 diffuse

B
7. Acetyl choline bind to receptors
Channel proteins open …Na+ influx

8. The post synaptic

neurone depolarised

175 / 270
 Cholinergic synapses( type of synapse which releases
acetylcholine as neurotransmitter)
1. An impulse arrives at the synaptic bulb .
2. In response to depolarisation at the presynaptic membrane , the VG channel proteins of calcium ions open
So Ca+2 diffuse into the cytoplasm of the presynaptic bulb / neurone
3. Ca+2 ions trigger the movement of vesicles towards the presynaptic membrane
The vesicles will fuse with the presynaptic membrane ,
4. Release of the neurotransmitter molecules into the synaptic cleft by exocytosis

5. The neurotransmitter molecules diffuse across the synaptic cleft

6. And bind to the receptors on the post synaptic membrane
7. The sodium ions channels open to allow diffusion of sodium ions into the cytoplasm of the post synaptic
neurone down electrochemical gradient

8. The post synaptic membrane is depolarised ( initiation of action potential )

9. The sum of all impulses arriving at the post synaptic neurone is greater than its threshold , then the impulse is
sent . ……action potential is set up in te post synaptic membrane
Allowing one way flow of information

10. Neurotransmitter molecules leave the protein channels / receptors and are broken down by an enzyme
11. The products diffuse back into the presynaptic membrane to be recycles into presynaptic neurone .
12. With the removal of neurotransmitters , this stops continuous depolarisation of post synaptic membrane /
post synaptic membrane is repolarised ……so making receptors available again.
176 / 270
Function of synapse

1. Transport information between neurones …as synapse is found between neurones .

2. Ensure one way transmission …..presynaptic neurone ( knob) contain vesicles that contain
neurotransmitters and only the post synaptic membrane has the receptors for neurotransmitters …so simply
any action potential would stop at this point .

Neurotransmitters

Excitatory neurotransmitters Inhibitory neurotransmitters

They open Voltage Gated Na+ They open Voltage Gated K+ channels OR Cl-
channels leading to depolarization of channels leading to hyperpolarization of the
the Postsynaptic membrane/ Postsynaptic membrane/ neurone.
neurone. Neurotransmitters released by inhibitory
Example: Acetyl choline neurone , stimulate ion flow that makes
Epinephrine /nor epinephrine them-inside of neurone more negative
….HYPERPOLARISATION ….this
decrease the potential difference makes
it more difficult to depolarise the
neurone .
177 / 270
Neurotransmitter …..acetylcholine

Acetylcholinesterase is needed to break down acetylcholine into acetate and choline , to be released
from receptors
choline diffuse back into presynaptic membrane so that choline is recycled into presynaptic
neurone .

Inhibition of enzyme

So acetylcholine concentration in synaptic cleft remain high

So acetylcholine binds to receptors in post synaptic membrane
Where sodium ions move into post synaptic neurone casuing depolairsation of post
synaptic membrane
Leading to Continuous stimulation / action potential in the post synaptic cell
Besides The presynaptic cell will run out of acetylcholine due to less recycle of choline

Why synapse act as a one way valve

1. Neurotransmitters are produced on one side of the synapse ( in the presynaptic Knob) …so the impulse
can move only across from that side
2. Receptors are found on the surface of the post synaptic membrane .

178 / 270
 Effect of drugs on the nervous system

Nicotine It mimics the effect of acetylcholine and binds to specific acetylcholine receptors in
post synaptic membrane ( bind to nicotine receptors)

Trigger an action potential in the post synaptic neurone .

But then receptors remains unresponsive to more stimulation for some time .

Nicotine cause increase in heart rate and blood pressure

Trigger release of another neurotransmitter …dopamine …..pleasure sensation

Highly addictive
179 / 270
 treannawirere
Lidocaine

Block the VG sodium channels

No influx of sodium ions into the neurone
No depolarisation
No neurotransmitters released in next synapse

npeirninotethe
No impulse reaching the brain
Til
A) Prevent you from feeling pain

B) use to prevent some heart arrthymias ( irregular heart beat ) ….block sodium channels
…..increase the depolarization threshold ….this reduces early or extra action potentials from
pacemaker

Cobra venom ( alpha cobratoxin):

Its toxic and often fatal in snake bites .

Binds reversibly to acetylcholine receptors in post synaptic membrane and neuromuscular junctions
Thus prevent prevent transmission of impulses across synapses including neuromuscular junctions
So muscles not stimulated to contract and gradually causes paralyses
In case toxins reach muscles involved in breathing it causes death ‘
Yet it can relax the muscles of the trachea and bronchi in sever asthma attacks and so save lives

180 / 270
Sensory receptors rent
at
sermyher.

it

It consists of one or more specialised cells ( not neurones ) that are sensitive to a particular type of stimulus
These cells usually synapse with a normal sensory neurone which carries impulses to CNS
Example retinal cells

Types of receptors Stimuli

Chemoreceptors PH level of blood , smell, taste

Mechanoreceptors Pressure , tension, gravity , movement

Photoreceptors Light ( visible light for human/ U.V light for insect )

Thermo receptors Change in temperature

How receptors work

Stimulus……..local change in permeability of the membrane of the receptor ……generator potential………action potential .
Stimulus ………received by sensory receptors ….open Na+ VG channels …where sodium ions diffuse / influx
into the cell ( sensory receptor ) …down their electrochemical gradient …..the membrane is said to be
deplorised …results in generator potential ( doesn’t obey the all or nothing law ) ……if large enough to reach
the threshold of sensory neurone …..so action potential occurs in the neurone ( obey all or nothing law )
181 / 270
Synapse

A) divergence : a single impulse from one neurone can be

conveyed to a number of neurones at a synapse

B) convergence : number of impulses can be compiles into

single impulse

In eye …..several receptor cells often synpase with a single sensory neurone …….if the
generator potential from an individual receptor cell is insuffecient to trigger an action
potential …..the generator potentials from several receptors may add together and
trigger an action potential ….known as convergence ….useful adaptaion for increasing
senetivity of a sensory system ( as in retina of eye ) to low level stimuli
Spatial summation

182 / 270
25/3 / 2023

183 / 270
 Differentiate between weak and strong stimulus

1. Nerve impulses are describes as all or nothing responses

2. There is a certain level of stimulus , which is the threshold. That triggers the impulse
3. Potential difference is below the threshold , no impulses generated , and above the
threshold value an impulse will be generated
4. The action potential is the same regardless of how much the stimulus is above the
threshold value ..
5. We can determine the size of the stimulus …by :
A) frequency of impulses passing in a unit time ….where the larger the stimulus , the more the action
potentials that are generated per unit time .
B) number of neurones carrying action potential . In eye
A weak stimulus …….result in a low frequency of
action potentials along sensory neurone

A strong stimulus result in a rapid stream of action

potentials being fired along a sensory neurone

Important to the eye ;

This makes the eye not only aware by light and dark
But also by degrees of light intensity and shades
184 / 270
The human eye

The eye pupil appears black because the choroid

absorbs light, preventing internal reflection of the light.

185 / 270
Structure of the retina
Outer segment with
vesicles ..contain rhodopsin
( opsin + retinal) Choroid

Inner most layer

Middle layer Outer most layer

1. Arrangement of retina appears back to front

2. The outer segment are next to choroid
3. Light has to pass through synapses and inner segments before reaching the outer segments containing the
visual pigments ( photoreceptors)
4. Light is said to pass by ganglion cell. ….then bipolar cell layers ….reach the photoreceptors .
5. Reason …..its about origin of the retina and the way eye is formed during embryonic development …
Back to front structure ….which is a reason why there is a b,ind spot …where all nerve fibres are gathered together
to pass through all layers of the eye to go to brain …..this means there is a spot where there cant be any sensory
reecptors .
186 / 270
 Rods Cones
Outer segment
Contains disc vesicles contain
Outer segment visual pigments Iodopsin
Contains disc vesicles contain ( need to be hit with more light to
visual pigments rhodopsin break down)

Inner segment packed with

Opsin Retinal ) light
( lipoprotein) absorbing derivative of many mitochondria
vitamin A )
and ribosomes
Inner segment packed with many
mitochondria to provide ATP /
energy for the synthesis of
rhodopsin .
and ribosomes

Number 120 million rods 6-7 millions

Peripheral parts of retina

Distribution Not found at the fovea In the center at the fovea

Every 3 / group of rods Every one cone cell synapse with one
Nerve connection synapse with one bipolar cell bipolar cell

Rhodopsin ( opsin + retinal ) Iodopsin ..

Type of pigments Respond to low light intensity giving black Respond to bright light and give great clarity of
and white vision vision and colour vision 187 / 270
 Light preception
1. In the rods we have photosensitive ( visual ) pigments are rhodopsin which absorb light
2. Light convert the Cis retinal into trans retinal ….( rhodopsin will change in shape )
3. This change in the shape of retinal …., which puts strain on the bonding between opsin and retinal, causes the rhodopsin
breaks into opsin and retinal .

4. This is refered to as bleaching …..the photochemical break down visual pigments

5. Opsin bind the cell membrane block Na+ VG channels
6. So no /fewer sodium ions enter the rod cells
7. Yet the sodium potassium pump continues working pumping sodium ions outside
8. Hyperpolarisation in rod cells/ membrane occurs .

Change from cis to trans retinal

z Rhodopsin
light sensitive pigment
+ retinal Opsin Generator
potential
Bleaching
If exceeds the threshold

Trigger action potential

In dark , Rhodopsin is resynthesised where trans retinal is

Nerve impulse along
converted back to cis retinal and join back to opsin to
optic nerve
form rhodopsin using ATP from mitochondria

188 / 270
1. Where the opsin uncouples
from the rod cell surface Dark Light
1. Absorb light , which
membrane
convert Cis retinal into
Trans retinal is converted into
trans retinal …break
Cis retinal to join to opsin again
rhodopsin into Opsin and
forming rhodopsin
retinal
2. Opsin block Na+ VG
2. Na+ VG channels open so
channels …no Na+ influx ,
Na+ ions influx
yet Na+ / K+ pump is
working pumping Na+
3. Depolarisation in rod cells /
outside the rod cell ..so
decrease Hyperpolarised .
inside become more
negative
4. Release inhibitory
3. Hyperpolarisation in the
neurotransmitter
rod
( GLUTAMATE )
4. no inhibitory
neurotransmitter
5. Cause the bipolar cells to be
( glutamate ) released .
hyperpolarised and so cant
5. Bipolar cells are
release excitatory
depolarised and release
neurotransmitter
excitatory
6. So no depolarisation in
Dark adaptation Light adaptation neurotransmitters
ganglion cells and no impulses
6. Depolarisation in ganglion
reaching the brain
cells …electric impulse to
brain 189 / 270
 Light adaptation
In the rods the the visual pigments is rhodopsin
which absorbs light
Light converts the Cis retinal into trans retinal ..( rhodopsin change its shape)
This change in the shape of retinal …., which puts strain on the bonding between opsin and retinal, causes the
rhodopsin breaks into opsin and retinal .
This is referred to as bleaching
Opsin binds with cell surface membrane …..blocking Na+ channels
So sodium ion channels close so rod cell membrane becomes less permeable to sodium ions and fewer sodium ions enter
into the rod cell .
Yet sodium potassium pump continues to work pumping sodium ions out of rod cell . So interior becomes more negative
than usual …..
So hyperpolarisation ( generator potential ) in the rod occurs leading to change in voltage

Reducing / no the release of glutamate / inhibitory neurotransmitter from rod cells

If the stimulus is large enough an action potential (depolarization) is formed in the bipolar cell
- Bipolar cells are now depolarized.
- Bipolar cells release excitatory neurotransmitter acting on Ganglion cells.
- Depolarization of Ganglion cells occur
and an electric impulse is transmitted to the brain. ( nerve impulse along sensory neurone /optic nerve to brain )

Notice : If the light stimulus is of lower intensity than the threshold of stimulation, then few bleaching of Rhodopsin
would occur and few Opsin molecules released. So, not all Na+ channels are blocked.
- The changes in Potential Difference across the Rod cell membrane are minimal, which means that the Rod cell
is not hyperpolarized and is still able to release the inhibitory Neurotransmitter Glutamate

190 / 270
 Dark adaptation
where the opsin uncouples from the rod cell surface membrane
Trans retinal is converted into Cis retinal
And cis retinal joins to the opsin again
forming rhodopsin
Using energyt from ATP ( produced from many mitochondria in the inner segments of rods.
Where ….in complete darkness the rhodpsin will have completely reformed from opsin and retinal so eye is fully
sensitive to low light intensity …..
This result in dark adaptation ( said to be dark adapted ) ..

Where the permeability of cell surface membrane to sodium ions increase

The Rod cell membrane has open VG Na+ channels and active Na+ pump.
Influx of Na+ through open channels causes depolarization.
Hyperpolarisation decreases

This depolarization stimulates the release of an inhibitory Neurotransmitter (Glutamate)

Neurotransmitter ( glutamate) is released

- Glutamate causes hyperpolarization of the Bipolar cell.

- No neurotransmitter released from Bipolar cells.
- Therefore, No depolarization of Ganglion cells and No impulses
reaching the brain
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 why u become almost blind when you walk from sunny street into a house ?
Once visual pigments has been bleach'ed …..rod cant be stimulated again until rhodopsin is
resynthesised
where the opsin uncouples from the rod cell surface membrane
Trans retinal is converted into Cis retinal
And retinal rejoins to the opsin again forming rhodopsin
Using energyt from ATP ( produced from many mitochondria in the inner segments of rods.

In normal light rods are entirely bleached and cant respond to low light intensity and eye is light adapted
After 30 mins ….in complete darkness the rhodpsin will have completely reformed from opsin and
retinal so eye is fully sensitive to low light intensity …..This result in dark adaptation ( said to be dark
adapted ) ..

This explains why u become almost blind when you walk from sunny street into a house
Where bright light has completely bleached rhodopsin that you need to see in the darker interior light
As rhodopsin reforem in your rods , your vision returns as your eye become dark adapted again

Where the permeability of cell surface membrane to sodium ions increase

Hyperpolarisation of the cell decreases
More inhibitory neurotransmitter is released
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 Importance of ATP in rods? Effect of some drugs / eye drops

ATP provides energy

Act on the nervous system of the eye ( iris)
To convert Trans retinal into Cis retinal
Causes the radial muscle to contract
And rejoins retinal to the opsin again
And thus allowing pupil to dilate
forming rhodopsin
And prevent pupil constriction
So allowing more light to enter
In light / effect of higher light intensities So can see more retina
The greater hyperpolarisation ……
less / no glutamate releases by rod cells Atropine inhibits the nerve impulses in
the parasympathetic system .
Greater number of action potential generated in the bipolar cells the sympathetic system is still
working
Increase frequency of action potentials this cause the contraction of the radial
Which is interpreted as more intense light by visual cortex / occipital muscles
lobe . and the circular muscles are not
stimulated or they are relaxed

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 Pupil reflex Circular muscle contract and radial relax to constrict eye pupil
Circular muscle relax and radial contract to dilate eye pupil
Allowing a change in size of eye pupil in response to different light intensities
Where antagonistic muscles have opposite effects / work opposite to each other
Sensory neurone Motor
Stimulus ……..receptor ………………………..CNS …………………effector ………..response
( optic nerve) neurone
Stimulus received by sensory receptors( rods / cones ) in retina in eye …….
so action potential occurs
Where reflex arc is formed
And impulses / action potential passes through sensory neurone
in the optic nerve to the relay neurone in brain …
then pass cross the motor neurone which is connected to radial muscles of iris.
allowing contraction of radial muscles ..allowing pupil to dilate …or the opposite

Bright light ' DIM light

[Link] muscles contract and radial muscles relax [Link] muscles relax and radial muscles
[Link] muscles arrange in concentric rings around the pupil and contract
radial muscle run radially . 2. Pupil reflex is the reflex contraction and
relaxation of the antagonistic muscle of the

÷
[Link] reflex is the reflex contraction and relaxation of the
antagonistic muscle of the iris . iris .
[Link] pupil becomes smaller/ constrict so less light enters the [Link] pupil becomes larger/dilates so
eye more light enters the eye

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28/3/2023
Habitation

Dr. Nihal Gabr

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 Habituation

A reduced response to a non threatening stimulus that is repeated

Its considered as a form of learning
Sea slug breaths using a gill in a cavity on the upper side of the
body , water passes through and is forced out through a siphon tube
at one end ….if you touch the siphon tube , the whole gill is
withdrawn intomthe body cavity as a defence mechanism ..however
as the sea slug. Lives in sea , the movement of water constantly
stimulate the siphon . The animal learns by habituation not to Becomes habituated after several
withdraw irs gills every time a wave hits it repeated stimuli on the siphon ..the gills
will no longer be withdrawn …

Mechanism of habituation:
1. Decreased responsiveness of the presynaptic neurone to calcium ions /
calcium ion channels dont open / reduced activity of calcium channels / reduced
influx of calcium ions

2. Less neurotransmitters fuse with presynaptic membrane

3. Less neurotransmitter releases from the presynaptic membrane
4. Less binding to receptors on the post synaptic membrane
5. Less depolarisation of the postsynaptic neurone .
6. Less action potential generated in the postsynaptic neurone ( motor )
Less impulses reach ( siphon ) 196 / 270
 Strength/ time of response
Importance / advantage of habituation:

1. Stimulus is ignored since its harmless / not threatening

2. Where less withdrawal of siphons save energy for other activities
3. Allowing gas exchange as well .
The organisms get used to repeated stimuli in their normal life . Number of times stimulus is given

Factors affecting how fast habituation takes place :

1. Frequency of the stimulus they are exposed to
2. Duration of stimulation
3. Strength of the stimulus

Plan an investigation using a snail

1. Get snails of same species ,age , gender and body size / mass
2. Place one snail on clean surface
3. Leave the snail till it fully emerge out from its shell
4. Used a mositured / wetted piece of cotton and touch between the eye stalk
5. Start your stop watch once it enters the shell and measure the time till the sail reemerge from the shell
6. Repeat the touching action 15 successive times and record at each time , the time needed for the snail to reemerge
[Link] validity ……touch with same strength each time , temperature , light intensity, humidity.
8. For reliability …repeat the whole process on 10 other snails and calculate the average . 197 / 270
Notice : habituation is not like synaptic accommodation,

Where synaptic accommodation, is caused by temporary exhaustion of neurotransmitter stores.

It is caused by a temporary depletion of synaptic vesicles that house neurotransmitter in the synapse,
generally produced by persistent high frequency neuronal stimulation.

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Check list
1. Describe the structure different parts of neurone and their functions
2. State the three types of neurones and compare sensory and motor neurones
3. Describe the difference between mono and poly synaptic reflex
[Link] the difference between spinal and cranial reflex
5. Describe spinal reflex in case of hand-withdrawal
6. Name the transport proteins involved in both resting and action potentials
7. Describe properties of membrane of axon
8. Describe how Resting potential is established and maintained .
9. Why resting potential requires energy

10. Describe depolarisation, repolarisation , hyperpolarisation , resetting frm

hyperpolrisation
11. Identify these stages in the graph
12. State the idea of all or nothing law
13. Describe how nerve impulse propagate in nerve cell / fibre
14. Importance of refractory period

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15. How action potential is transmitted along the myelinated neurone
Check list
16. Factors affecting the transmission of action potential
17. Explain role of myelin sheath
18. Label synapse
19. Role of neurotransmitter
20. Cholinergic synapses( type of synapse which releases acetylcholine as
neurotransmitter)..describe how depolarisation occurs in post synaptic neurone .
21. types and role of different types of neurotransmitters
22. Why synapse act as a one way valve
23. Role of acetylcholinesterase
24. Explain what happens upon Inhibition of enzyme
25. Explain the effect of lidocaine / nicotine / cobra venom on nervous system

26. Describe how receptor works

27. How to differentiate between weak and strong stimulus in eye ?
28. Label different parts of the eye
29 . Why pupil appears dark ?
30 .label parts of the retina….and rods and cones
31. Explain how retina is arrangement appear back to front
32. Why blind spot has no photoreceptors .
33. Compare between rods and rods
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34. Describe action of rods and cones Check list
35. Compare between dar and light adaptation
36. why you become almost blind when you walk from sunny street into a house ?
37. Importance of ATP in the rod cells
38. Describe pupil reflex in light and dark including
A) action of antagonistic radial and circular muscles
B) draw the arrangement of muscles
C) reflex arc .

39. Role of some eye drops used in examining the retina .

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 Topic 8B
Coordination in
animals and plants

Dr. Nihal Gabr

202 / 270
Part 1
Brain structure
Brain imaging
Nervous system structure

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 The formation of the brain
Basic brain pattern

In some vertebrates , the brain

remains simple with these parts for

a Brain ventricles smelling and sight

Forebrain Hindbrain forms

Mid brain
Contains the olfactory cerebellum and In mammals , the brain becomes
lobes and in higher contain optic
vertebrates forms cerebral
medulla extremely complicated and develop
lobes
hemispheres cerebral hemispheres ( cerebrum)

The brain is made of a combination of

grey matter ( neurone cell bodies )
and white matter ( nerve fibres) .

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 A Cerebrum ( two cerebral hemispheres )
Brain structure Control the voluntary behaviour including movement
Site of intelligence , learning , feel emotions , memory,
personality, think, ability to see , speech

Made of bundle of E
neurones ( fibres) Corpus
Connects the right a
callosum
and left
hemispheres
D
Hypothalamus
&
-Plays an important part in P
homeostasis
B'
1) thermoregulatory center
C Medulla oblongata
2) osmoregulatory center Controls the balance
It contains reflex
- connected to pituitary gland to centers ..to control and coordinate
control the release of breathing rate , heart rate , movement
hormones . blood pressure , and
peristalsis
Regulation of
cardiovascular /
respiratory system

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 They receive
and interpret
stimuli from
-

To send impulses to the effector sensory

-

neurones or
organs

Memory ,
thinking ,
learning , IQ,
feelings

Motor areas in frontal lobe ….send impulses to the effector

Pre frontal association area ……in front of frontal lobe …..memory , thinking , learning , IQ , feelings
Sensory area …parietal lobe ……. They receive and interpret stimuli from sensory neurones or
organs …sensation
Visual area …….occipital lobe ….concerned with processing inputs from the eye
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 Nervous system
CNS ( central nervous system ) PNS ( peripheral nervous system )

Brain Spinal cord Sensory neurones Motor neurones

Receives and Conduct signals to Carry impulses from the receptors Carry impulses out of the
in sense organs to CNS CNS to the effectors
process sensory and from the
information brain , control
Initiate response , reflex activities
stores ,
memories , Somatic nervous system Autonomic nervous system
generate thoughts Voluntary nervous system Neurones to smooth muscles ,
and thinking Under the conscious control glands , cardiac muscle, not inder
Involving the cerebrum ( neuroses to conscious control
skeletal muscles ) Example : control of heart rate ,
breathing rate , dilation and
constriction of iris / blood vessels ,
movement and secretions in gut

Sympathetic-nervous system Para sympathetic nervous system

Fight or flight Rest and digest

Neurotransmitter is noradrenaline Neurotransmitter is acetylcholine
Increase Heart rate , breathing rate Decrease heart rate , breathing rate
Dilates the eye pupil …
Constrict the pupil
Constrict bladder sphincters
Dilates and relaxes sphincters 207 / 270
 Parasympathetic Sympathetic

Similarity Both have myleinated preganglionic fibres that leave the CNS
and synapse in a ganglion ( collection of cell bodies outside the
CNS) with unmyleintaed post ganglionic fibres

In sym …..the ganglia are very close to the CNS/ spinal cord ,
Difference
so the pregnglionic fibres are short and the postganglionoic
fibres are long .

In para …….the ganglia are near to or in the effector organ /

far away from spinal cord, so pre ganglionic fibres are very
long and the post ganglionic fibres are very short

↑ Myelinated
CNS
Y mmm.X
wwwwr

,un myelinated post Preganglionic nerve ,un myelinated post

ganglionic nerve fibre fibre ( long ) ganglionic nerve fibre
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 Brain imaging are brain imaging methods
wit high resolution

Studying Importance of brain imaging :

human 1. Detect any abnormality in brain ….. example bleeding , density change .
brain 2. Detecting the type , size , location of abnormalities ( tumors, oedema ,
stroke, hemorrhage )
3. 3. Follow up effective of a treatment by repeated scans and comparisons
4. Looking for surgical accessibility ( according to site / size ) .

Why abnormalities in different parts of brain cause different symptoms :

1. different regions of brain affected .

2. Different areas of brain have different functions
3. Symptoms depends on region of brain affected
4. Where different type of abnormalities cause different symptoms

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1. CT scan ( computed Tomography )
[Link] X ray
[Link] of the brain tissue determines the ability of rays to pass
through . Where each beam is reduced in strength by density of
tissue it passes through . ..then X rays that pass through tissue are
detected and measured and used by a computer to produce a cross
sectional image of a thin slice through body .
[Link]’t allow the observation of brain in action
4. Provides image of both hard ( like bones ) and soft tissue with or
without contrast medium but much less useful in providing or in
producing images of soft tissue

Advantages :
1. Identify major structures of the brain
2, detect problems such as brain tumors , bleeding , aneurysms
3. Cheap and available.

Disadvantages :
1. Doesnt allow observation of the brain in action , only showing structures
2. Cant detect smaller abnormalities / lesions due to low resolution
3. Hazard of using X rays ( carcinogenic)

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2. MRI magnetic resonance imaging
Mechanism :
1. Use magnetic field and radio waves
2. Which excites proton in water ( as the human body is so much made of water ) where hydrogen atoms produce
MRI signals ….and computer analyse the signals produced. and produce an image .
3. The way they respond depends on the amount of water in the soft tissue

Advantages of MRI over CT scan

1. Better resolution than CT scan

2. More details seen / sharper image ( finer details seen)
3. Can diagnose brain injuries, strokes , tumors and infections of the brain or the spine .
4. No use of X rays
Safer with less risk to cell damage or mutation
So can be used more often
And can be used by pregnant women

Can show organs , bones , muscles , and blood vessels

Disadvantages :
1. MRI is noisy ..stressful
2. Head must be kept completely still as
movement reduce accuracy of image .
3. Expensive 211 / 270
fMRI functional magnetic resonance imaging
Mechanism :
1. The basis of fMRI depends on using magnetic field and monitoring the absorption of oxygen in
different brain areas
2. It differentiates the oxyhb from the deoxyhaemoglobin…….. Deoxyhaemoglobin absorb wave signals
While oxyhaemoglobin reflects the magnetic field / radio-waves ( doesn’t absorb) .

3. Where blood flow to an area of the brain which is more active

-More oxhaemoglobin is delievered to supply oxygen to active cells
-For aerobic respiration
-So an active area of the brain absorb less energy ..appear white
-While less active area appear black
-Showing activity of brain in real time

Sum up for the mechanism :

[Link] shows brain activity
[Link] measuring uptake of oxygen
[Link] areas of brain gets more blood …more oxygen
Lower signals mean
[Link] oxyhaemoglobin is delivered to supply oxygen to active cells
higher brain activity
[Link] active areas appear light / white

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Advantages of fMRI
[Link] can allow brain activity to be seen in real time
[Link] uses radio waves / magnetic field …as MRI
3. Increase supply of oxygenated blood in active areas
4. these regions with oxyhaemoglobin reflects / doesnt absorb fMRI signal
5. So seen as white areas / light up on the image ….
6. All advantages of MRI (+ high resolution….as MRI + safer. ….as MRI )

During memory test

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214 / 270
PET scan :positive emission tomography scans
4) PET scan ( positron emission tomography )

Mechanism

1. The patient is given radioactive material ( radio tracer which is a radio

active isotope that emits positrons ) containing glucose .
2. This radioactive material incorporated into glucose is absorbed by more
active cells / neurones to be used with the increased respiration.
3. As they require increased supply of glucose
4. -The increased radioactivity emitted from areas with high metabolic rate
can be detected by the PET scanner…..in other words positrons emitted
from glucose produce gamma rays that are detected and converted into
an image .
—So for example cancer cells absorb much more radiotracer than normal cells ..
—Areas of brain less active / dead as a result of disease such as Alzehieme’s that cause
dementia) absorb less of the radioactive tracer than expected .

Advantages:
- It helps to diagnose conditions that affect cell activity such as areas with cancer growth (more
active) or brain diseases like dementia.
- Provides a very detailed image helping in diagnosis and and show how parts of brain actually
working
-And can be used to plan surgery by providing a 3D image to surgeons of the area of brain that are
affected .
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 Chemical balance of the brain

Communication between neurones around the body and in brain depends on delicate balance of naturally
occuring neurotransmitters ( dopamine and serotonin )
Imbalance in them result in both mental and physical symptoms .

Coordination of movement:

1. The motor commands / orders arises from the motor areas in brain ( cerebral
cortex ) .
inalganglich
2. The basal ganglion determines the speed of movement
3. This determination of the speed depends / occurs in response to two
neurotransmitters:
A) dopamine ( secreted from Substantia Nigra ) : speed up motor command

Area of the midbrain involved in the control and coordination of

movement ….affected by Parkinson’s disease.

B) acetylcholine ( secreted from cholinergic area) : slow down the motor command .

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 The blood brain barrier

[Link] capillaries in brain have very tight narrow endothelium ( narrow pores)
[Link] protects the brain from many pathogens in blood as it makes it difficut for the bacteria to cross into
brain and cause infection .
3. However, this is a disadvantage in terms of many therapeutic drugs being unable to reach / enter the
brain .

So , drugs do affect the brain usually active at the synapses where they can target
several stages ( enzyme / re uptake / binding to receptors/ ca+ channels )

Parkinson’s disease

Area of midbrain involved in control and coordination of movement is affected by Parkinson’s disease

Risk factors
Genetic factors ( weak link )
Environmental factors ( repeated head trauma , herbicides , pesticides )

Mechanism of disease

Gradual damage. Degeneration to nerve cells in Substantia NIGRA ….which

normally responsible for the release of dopamine .
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Why the reduction in dopamine by presynaptic neurones affect the motor action ?

1. Fewer dopamine molecules to bind to the receptors / ligand gated sodium

channels .
2. On the post synaptic membrane
Bring
3. Initiating fewer action potential in post synaptic neurone
4. So fewer impulses sent to parts to brain controlling the motor function / muscles

Symptoms

1. Tremors ( shaking )
2. Slowness of movement
3. Stuffiness ( rigidity ) of muscles …hard to stand up or turn in bed
4. Poor balance , difficulty in walking
5. Difficulty in breathing
6. Difficulty in speech ….depression

In Parkinson’s disease the dopamine producing cells in the motor cortex die .

Treatment

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1) L DOPA

- as the person with Parkinson’s disease normally has low level of dopamine.
- giving dopamine is not effective , as dopamine is too large to pass the blood brain barrier
- L dopa the precursor of dopamine , so it can enter the brain due to its small size .
- inside the brain ..L Dopa is converted into Dopamine in brain tissue.
- Dopamine bind to receptors on post synaptic membrane . triggering an action potential at synapse .
Restoring the control of muscle movement

2) Dopamine agonists :

- can cross the blood brain barrier

- They stimulate Dopamine receptors in brain synapses . (Mimic the effect of dopamine .
-Dopamine binds to receptors on the post synaptic membrane …..triggering an action potential

3) MAOB inhibitors

- MAO ( monoamine oxidase B) is enzyme that breaks dopamine .

- MAOB inhibitor bind and block the MAO enzyme , so dopamine is not broken down
- dopamine bind to the receptors on post synaptic membrane .

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Depression

Decreased level of serotonin ( neurotransmitter) .

Symptoms ( SIGE CAPS )

Symptoms :
1. Sleep
Increase in sleeping hours 1 unable to enjoy life
Decrease in sleeping hours 2. Unable to relate to others
3. No self esteem
2. Interest ..lack of interest in enjoyable stuff .
4. Sense of irritability
3. Guilt feeling 5. Restless
[Link] …lack of energy 6. Thinking of committing suicide
5. Concentration loss.
6. Appetite
Decrease
Increase
7. Psychomotor retardation
8. Suicidal plans

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 Treatment

2) Psychotherapy
1) treatments with drugs
CBT ( cognitive behavioral therapy )
A) TCA ( tricyclic antidepressant ) …..SNRIs Discuss the problems with patients .
Increasing level of serotonin and nor adrenaline in brain .
They block reuptake channels of Serotonin and Noradrenaline. (SNRIs)
SNRIs ….serotonin and nor epinephrine re uptake inhibitors

B) SSRIs ( selective serotonin reuptake inhibitor ) :

- they block the re uptake channels of serotonin in the presynaptic membrane .
- more serotonin in synaptic cleft .
- more binding to the receptors on the post synaptic membrane .
- more action potentials in post synaptic neurone .

C) MDMA ( 3, 4 methylene dioxy N methyl-amphetamine ) ( ECStasy) :

• same as SSRIs….illegal
It affects the hypothalamus so that it secretes more ADH so effectively
• euphoria , confidence , ecstasy
stops the kidney from producing urine ( oliguria ) and can lead to
Side effects : problems if the person keeps drinking water in an attemp to stay
1. Affect hypothalamus ….hyperthermia hydrated and cool down .

2. Increase ADH
3. Medulla oblongata…increase in heart beats ( tachycardia ) , increase in blood pressure ( hypertension )
221 / 270
 Drug testing

2. Preclinical phase which involves testing on animals or human cells …..to monitor the toxicity and see how it
works in whole organisms .
3. Clinical phase 1 , Drug being tested on healthy volunteers …..to monitor the safety and exclude major
unexpected side effects
4. Then review by independent scientists to see if work can progress for phase 2
5. Clinical phase II, Tested on small number of patients ( 500 to 1000) using appropriate concentration /
dosage .
6. Clinical phase III , Drug is being tested on patients with larger group over 5000 to monitor te effectivness
and safety
( using placebo and double blind trial for both phase II and III……
7. Where a number of patients should be placed randomly into two groups
A) one group will receive the drug containing chemical compound
B) and the other will reecive the placebo ..acting as a control group taking the drug without active ingredient
for comparison and to assess the magnitude of psychological effect .
8. Double blind , where neither the doctor nor the patients know who is taking the real drug to remove bias .
9. Statistical analysis and test for significant differences

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Chemical coordination systems in plants
[Link]

1. Response in venous flytrap

Sensory hair cells …touched

2 touched within 35 seconds …action potential spread over
the leaf

2. Phototropism
Plant parts respond to light
A) Light is coming from one side ( unidirectional light )
Auxins to be redistributed in the shaded side
Stimulate the cell elongation
Bending towards light

B) light is coming from both sides , auxins are equally distributed on both sides
So grow straight up

C) if no light
Grow straight up ( more vertical growth ..where etiolation occurs .
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 Phototropism… Auxins ( IAA) 5
Expansins
Cell wall

1. Auxins are secreted from the meristem ( growing tip of the

3 4
shoot ) , shoot tip act as photoreceptors to light causing the 7

redistribution of auxins
2. the auxin diffuse down wards to reach zone of elongation
( shaded side ) stimulating cell elongation .
Cytoplasm

3. Auxins bind to receptor in the cell membrane .

4. Auxin stimulate proton pumps in the cell membrane to be
actively transported ..the hydrogen ions from the cytoplasm into the
11. Causing cell walls to
space in the cell wall .
stretch allowing parts to
5. Cell wall become acidic ( decrease in PH )
grow in size /Causing cell
Activate proteins ( expansins ) and weaken the cell wall , temporary
elongation
break / disrupts hydrogen bonds between cellulose microfibrils and
dissolve pectin .
12. This continues until
6. Loosening cell wall
auxin are broken down .
7. Stimulate the potassium ions to enter the cells
Shoot grow towards light
8. So decreasing the water potential
( incase of unidirectional
9. So water will enter by osmosis
light .
10 . Causing an increase in turgor pressure

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225 / 270
 summary
-
Auxins are secreted from meristem ( produced from growing tip pf the shoot )
In case of unidirectional light …cause redistribution of auxins
Diffuse down its concentration gradient to the shaded side to reach zone of elongation
Stimulate cell elongation
A) auxin IAA binds to receptors on cell surface membrane .
B) stimulate the proton pump in the cell membrane to pump hydrogen ions from cytoplasm to intercellular
space in cell wall
C) cell wall will become acidic ( decreasing pH ) …activate some enzymes
D) activate protein ( expansins) where it weakens the cell wall by disrupting the hydrogen bonds between
cellulose microfibrils
And dissolve pectin
Loosening cell wall
E) potassium ions to enter the cells …so decreasing water potential ..so more water will enter by osmosis
Causing an increase in turgor pressure
Cell wall stretching allowing parts to grow in size in shaded side
Cells become longer
Curvature ./ beniding of shoot towards light .

Tropism
Plant parts ( shoot / root ) to bend towrads or away
from a stimulus ( light / gravity)
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17/4/2023
Part 3

Dr. Nihal Gabr

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Gibberellin
Aleurone layer

-
2

Embryo p
Gibberellin
Endosperm
Amylase
I 3

Gibberellin
Starch Maltose
Maltase
v

Glucose
They are growth regulators
⑧ Affect internodes of stems ,
stimulating elongation of the
growing cells
1. Water is absorbed by the seed
They also promot the growth of
2. Stimulate the production of gibberellin by the embryo within the seed
3. Giberrllin diffuse into the aleurone layer
· the fruit .
Involved in breaking dormancy in

4. Stimulate the production of amylase seeds and in germination …by

stimulating production of amylase
5. Amylase diffuse and move to the endosperm cataylse the braek doen of starch
into maltose
6. Then maltase stimulate the break down of maltose into glucose
7. Glucose transported into the embryo , providing energy as the embryo begins
to work
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 Plant hormones vs animal hormones

Similarities • They are both chemicals

• Both bind to receptors on cell membrane .
• Both control gene expression ( act as / activate TF)
• Both transported away from production site
• Both are made inside the cells

Differences

Animals hormones are transported in blood

Plant hormones move by diffusion

Plant hormones are slower in action , yet some animal hormones are faster

Some animal hormones have shorter term effect …( duration of effect )

All plant hormones are involved in growth / cell elongation , but animal hormones have many other
roles not just affecting growth .

Animal hormones are produced from glands but plant hormones are produced from different plant
tissues

229 / 270
Where the leaf has photoreceptors phytochrome

There are two main type of light:

A) Red light : bright light / Day time ( 660 nm )
B) Far Red Light : moon light / Dark / Night ( 730 nm)

• The light receptors in the plant known as PHYTOCHROME

• Phytochrome is a blue green pigment ( mainly found in leaves ) that exist in 2
interconvertible isomers / forms

A) Phytochrome Red ( PR) …..Pr ( P660) absorb red light , is an inactive form
B) Phytochrome Far Red ( PFR) ….Pfr ( P730) absorb far red light is physiologically active .

The absorption of light by one form , will convert it reversibly into another form

Absorb red light Far red light

( 660 nm ) (730 nm )
More at day time More at night
230 / 270
 • as seed germinates , it forms Pr ( inactive Phytochrome )
• Seedling start to emerge from a seed underground , it contains Pr
only , as it has not been exposed to light

If it remains Pr ( inactive ) form Pfr

Show typical characteristics of etiolation :
Pr
1. Rapid stem lengthening
Stimulation to the internode growth ( searching for light )
2. No leaf growth
3. No chlorophyll
4. Little root growth

A Once the plant is exposed to light B Continue in the dark , it will

continue etiolation and die
Pr is converted to Pfr ( active phytochrome )
due to use up of storage of
Pr absorb red light and converted into Pfr
starch / glucose
Pr
1. Inhibit lengthening of internodes slowing down internode growth
2. Stimulate the leaf development
3. Stimulate the production of chlorophyll
4. Leaves open and carry photosynthesis
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Effect of phytochrome on germination
Proven by an experiment

1. Red light source and expose a group of seeds to red light

• . Observe ….temperature start to increase …indicating an increase in enzymatic
activity of seed germination is happening

2. Far red light ( another light source ) is applied to seeds

Temperature decrease …enzyme activity decrease as germination is inhibited

Explanation • PFR ( active phytochrome ) is responsible for germination of certain types of seeds
• This means that REd lights stimulate germination , while far red light inhibits
germination
• The one exposed to red light …Pr is converted into active Pfr ( active phytochrome )
where PFR stimulate germination
• And the Pr inhibits the germination
• Yet the effect of light is reversible

232 / 270
So during day time most of the phytochrome in a plant is in the far red form pfr …if night period is long
enough , all phytochrome is converted back into red form Pr.

·
Stimulate germination
Inhibit germination ( stimulate chlorophyll
production)
No chlorophyll

Length of the time it takes for one form of pigment to be converted into another depends on light intensity

In low ( in dark ) Takes minutes

Pfr to be converted to Pr SLOWLY , but no Pr is converted back
Pfr stimulate the germination / Pr inhibit germination
Level of Pfr become too low to stimulate germination / level of Pr becomes too high to inhibit
the germonation
Pr is a more stable form of pigment .. but its the Pfr that is biologically active

In light Takes few seconds

The higher the light intensity the more the Pfr produced at a faster rate

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Phytochrome ( Pfr ) act as a transcription factor
Involved in switching gene on / off
Mechanism of action of phytochrome

1. Recombinant DNA ( gene coding for the production of phytochrome + GFP ( green fluorescent
protein ) acting as a gene marker )
2. The hybrid gene is inserted into plant calls …..they were able to produce plants with fluorescent
phytochrome .
3. Some seed were kept in the dark ….fluorescence linked to the Inactive Pr …was detected through out
the cytoplasm of the cells
4. Then exposed to red light …the labelled Pr is converted into labelled Pfr and the fluorescent Pfr moved
into the nucleus of cells

So how Pfr works

1. Pr is converted to nPfr in presence of red light

2. It moves ( Pfr ) to the nucleus through pores in nuclear membrane
3. In nucleus , it binds to a nuclear protein (PIF 3) phytochrome interacting protein
4. PIF 3 is a TF
5. PIF 3 binds only to Pfr ( doesn’t bind to Pr)
6. PIF3 only activates the gene transcription and the formation of mRNA when its bound to Pfr
7. activated genes control different aspects of growth and development in plants

234 / 270
 .seeds
PFR needed for germination
Mechanism

235 / 270
 The amount of time that an organims is exposed to light during a 24 hour period is called
photoperiod …affects the flowering activities of plant .

SDP s ( short day plant ) Pr Winter plants

Flowering occurs when day time is short and night as long such as rice and cotton
In SDPs …..Pfr ( active phytochrome ) inhibits flowering

[Link] the leaf has photoreceptors phytochrome

[Link] staying in the dark for enough time , allow enough stimulation
3. PR absorbs red light to be converted into PFR
SDPs PFR absorbs far red light and converted into PR
So relatively low Pfr levels
PFR is converted into PR slowly (these plants need a sufficiently long dark period to allow
maintained
Stimulate flowering PFR to reach critical (low) concentration ;
Stimulate release of florigen
Plant transport system carries it 4. Flowering is stimulated when the PFR is in low concentration / PR is at high
to flowering buds / sites
concentration
5. By releasing Florigen .
6. Transport system in plant carries it to the flowering buds / sites

236 / 270
LDP s ( long day plant ) Pfr

Summer plants , the situation is reversed , where high levels of Pfr stimulate flowering :

Short nights , no enough time for sufficient conversion of PFR to PR

↓ 4 So relatively little PR and high concentration of PFR during day time

High concentration of PFR stimulate flowering by stimulatingnthe release
of Florigen .
Stimulate flowering by
inducing the release of
florigen

DNP s ( day neutral plant ) are unaffected by length of day …known as day neutral plants
( DNPs) like the growing in tropic regions where day length is
same all year round .

DNP : day neutral plants

Where tropical regions the Pr and Pfr are similatr all year round
These plants don’t depend on Phytochromes for Flowering.
- Flowering occurs when they reach a certain size.

Florigen is plant hormone produced in response to changing levels of phytochromes

And plant transport system carries it to flowering buds .

237 / 270
Rec
E

Leaf is exposed to the right amount of light …..a particular mRNA is produced
Transcribed from a gene FT gene ….so its called FT mRNA
FT mRNA can move from one cell to another through plasmodesmata ……

Is chemically known as florigen

238 / 270
Why flowering depends on photoperiods and not any other abiotic factor like temperature ?

1. - Photoperiod shows a regular pattern of seasonal variation (Length of day time

( photoperiods ) changes to set pattern ( like always short days in winter and long days in
summer)

2. - This ensures that all members of the same species produce flowers at the same time
to increase the chance of pollination.

3. Also , this occurs simultaneously with other important biotic factors like the presence
of pollinators .

4. Yet , unlike other abiotic factors such as light intensity and temperature ( less regular
stimuli ) that shows fluctuation and changes through out the day .

239 / 270
 Topic 6 -

Gene technology-
i

8C I
-

Dr. Nihal Gabr

240 / 270
1/4/2023
8C genetic engineering

241 / 270
 Genetically modified organism……organisms that have genome ( DNA ) altered by genetic engineering

Scientists developed GMO …organisms have desirable features .

GM bacteria ……..insulin and growth hormone

Transgenic organism …….contain recombinant DNA GM Plant
Resistant to herbicides
Change Genes Beta carotene

Genetic engineering

By taking a gene from one organism and inserting it into

another organism .
Restriction
1. Gene
Reverse transcriptase
2. Many copies PCR
3. Vector ……
4. Join ligase
5. Promotor and gene marker

242 / 270
 The process of making a protein using genetic engineering has a number of stages

A Step 1 1. Obtain / synthesis the desired gene

A) reverse transcriptase B) restriction enzyme

Use RNA as a template to form Extracted from bacteria ….cut specific base
sequence ( restriction site / recognition site)
DNA
( reverse transcriptase produced by Cut double stranded DNA at a specific

retrovirus) recognition site leaving sticky ends

Mature mRNA with no introns +

easy to extract

1. A cell readily produce protein is

selected
2. They have large quantities of the
required mRNA which is extracted .
3. Reverse transcriptase is used to
make a single stranded cDNA
( complementary DNA) .
4. Then use DNA polymerase to make
another DNA strand , the double
stranded DNA is the required gene . 243 / 270
Step 1 1. Cut the gene of the desired protein using Restriction Endonuclease enzyme ( or obtain
the desired gene using Reverse transcriptase enzyme which acts on mRNA )

Step 2 Make many copies of the desired gene using pCR using
Taq DNA polymerase .

Step 3 Vector which is the plasmid removed from the bacteria and cut open using the same specific
restriction enzyme
Which leave sticky ends …which has complementary base sequence to sticky ends of the
gene .

Step 4 The amplified gene is mixed with the cut plasmid ( after adding promotor and gene
marker ) and DNA ligase link the sugar phosphate back bone and plasmid producing
a recombinant DNA ( ligase joins the gene to plasmid )

244 / 270
 Add a gene marker to the bacterial plasmid …gene coding for resistance to
Step 5
specific antibiotic / gene coding for a fluorescent protein ( GFP) / gene that
makes the bacterium dependent on a particular nutrients

Gene Gene of
Promotor
marker interest
Transcription factor / RNA polymerase
As the gene has to be inserted next to promoter
To identify the transformed bacteria
For TF to bind and initiate transcription.

. Identification of host cell that has successfully taken up the gene by using GENE MARKER

1. Make the fluorescent protein easily seen using UV light

Gene marker 2. Gene which causes the bacteria to become resistant t antibiotics
3. Makes the bacteria dependent on a particular nutrient .

Replica platting
We use replica platting to identify recombinant cells .
Growing bacteria on agar plates with different media .
This allows us to identify colonies that cant survive without a particular nutrient .
These are the bacteria that have been GM .
245 / 270
Transformed + non transformed

Culture the transformed bacteria over Nutrient medium.

Step 6
Allow large scale production inside a fermentor

246 / 270
 Identifiocation of the host cell has successfully taken up the gene of interest using
GENE MARKER ( transformed bacteria ) :

A GFP ( green fluorescence protein )

Easily seen using U.V light

B Making the bacteria dependent on a particular nutrient .

C Gene which cause the bacteria to become resistant to the antibiotics

Ampicillin
Tetracycline resistance
* C
resistance Normal plasmid of

Insulin gene had been inserted into the

E
bacteria

Gene of
interest plasmid at a point in the gene for
*
( insulin) tetracycline resistance V ~ A
Normal plasmid of
bacteria

1. Culture bacteria on an agar plate containing ampicillin antibiotic , where the plasmid containing
resistant gene to ampicillin will cause the bacteria with these plasmids to survive ….excluded C .
2. To identify the bacteria with recombinant DNA , add the bacteria using sterile velvet on an
agar plate containing tetracycline …so the transformed bacteria with recombinant DNA wont
grow on the plate containing tetracycline 247 / 270
Why use of antibiotic resistance gene as gene marker is not successful / not used anymore ?
1. Risk the spreading resistance to other bacteria …
2,. So antibiotics become no longer effective .

Explain the role of restriction enzyme in genetic engineering

[Link] restriction enzyme

[Link] to cut gene out of animal DNA
Cut double stranded DNA at a specific recognition site leaving sticky ends
[Link] many copies of the desired gene using pCR using DNA polymerase .
[Link] which is the plasmid removed from the bacteria and cut open using the same specific restriction
enzyme …[Link] produce sticky ends .
[Link] amplified gene is mixed with the cut plasmid ( after adding promotor and gene marker ) ..where hydrogen
bonds formed between bases at sticky ends.
7. and DNA ligase link the sugar phosphate back bone and plasmid producing a recombinant DNA ( ligase
joins the gene to plasmid )

Explain how cells / organism can be genetically modified ?

[Link] restriction enzyme
[Link] to cut gene out of DNA…….( gene involved in making ……..is isolated / obtained using reverse transcriptase from
mRNA/ synthesise gene using data base )
[Link] is needed which is the plasmid / virus used / micropipette injection/ gene gun/ liposomes .
4. Insert the gene into vector
5. and DNA ligase link the sugar phosphate back bone allowing incorporation of gene
6. Insert the vector into …….using heat shock/ gene gun/ microinjection .
248 / 270
 GMO
1. Gene
A) cut the gene using restriction enzyme
B) obtain the gene using reverse transcriptase where mRNA act as template to make cDNA
C) synthesizing gene using data base

2. Vector …..plasmid / virus / liposome ……….micropipette injection / gene gun

Insert gene into the vector

3. If vector is plasmid …DNA ligase sugar phosphate back bone

4. Insert the vector into the host cell …using heat shock / gene gun / microinjection

Insert gene
Host cell is bacteria

249 / 270
250 / 270
Steps. For genetically modified crop ( golden rice )

[Link] the gene involved in making beta carotene in bacteria / synthesis the gene using database / obtain nthe
gene using reverse transcriptase
2. Use restriction enzyme
[Link] to cut beta carotene gene out of DNA of bacteria
[Link] is needed which is the plasmid / virus used / liposomes .
4. Insert the gene into vector
5. Plasmid ( recombinant DNA) / vector put Into rice embryos by heat shock / gene gun / microinjection .
7. Grow rice into adult plants and select the modified rice plants with high yield of beta carotene .

251 / 270
How can u insert a recombinant DNA into other cells

( plasmids , virus, liposomes , microinjections, gene gun ) vectors.

Vectors transfer the required gene , with any marker genes , into new cells

Using virus

- Using Viruses as vectors: viruses bind to receptors on the host cells and insert their genetic material inside the
cell.

Challenges :
1, can cause an immune response in some people as other pathogenic organisms
2. Small packaging capacity / can carry small amount of DNA.
3. Low probability of integration into host genome .
4. Can cause mutation in host DNA / gene insertion disrupts gene function.

B. Using liposomes ( liposome wrapping)

a liposome is a sphere formed of phospholipid bilayer that can fuse with the cell membrane of target cell
and release its contents (recombinant DNA) inside the cell. This is known as Liposome wrapping.

Cause fewer side effect and less potential immune responses ….even
though not very effective at transferring (DNA Challenges : low ability to
add genes into target cells )

252 / 270
Microinjection :

Use a fine glass micropipette to physically inject the desired DNA into a fertilsed egg

Not very efficient because many cells have to be injected before one
accepts the DNA successfully …yet this method has resulted in most
successful transgenic animals .

Gene gun

Shoot a DNA carried on a very small gold pellets into cells at

high speed
Some cells survive this treatment and accept DNA as part of
the genetic material .

253 / 270
Knock out organism

A knockout, as related to genomics, refers to the use of genetic engineering to inactivate or remove one or more
specific genes from an organism. Scientists create knockout organisms to study the impact of removing a gene from
an organism, which often allows them to then learn something about that gene's function

Knock out organism …..is an organism with one or more gene silenced ( knocked out) so no longer works
A) to identify the function of the gene
Genome sequencing identify many genes , but yet scientist dont know the function of the gene in an organism.

B) to investigate disease and test potential treatments . …

Knock out gene coding for non functional protein in human …to creat animal models of the
disease ..these animals can be used for understanding human diseases and ways of treatment .
Where you can test drugs which are unethical for use with humans
Larger sample can be used in testing

Suggest the advantage of using mice as a knock out model compared with human model

Control genetic make since human shows genetic variation

Thus allowing one gene function to be investigated
besides mice reproduce quickly so get quicker results
Gene knock out ….complete elimination of gene from an
Where you can use drugs which are unethical for use with humans organism …no longer works
Larger sample can be used in testing Knock down …reduction of the gene expression
254 / 270
Drugs from genetically modified organisms

A How can u produce insulin from genetically modified bacteria

1. Extract mRNA for insulin from pancreatic beta cells .

2. Then mRNA is incubated with the enzyme reverse transcriptase ( obtained from retroviruses ) .
3. Using mRNA as a template to make cDNA
4. Then cDNA is converted into double stranded DNA molecule using DNA polymerase to assemble nucleotides
5. Where the sticky ends are created using restriction endonuclease and the plasmids are obtained and cut using
same restriction enzyme ( EcoR1) …leaving complementary sticky ends .
6. Then mix the insulin gene with plamsid
7. Some of the plasmid sticky ends pair up with the sticky ends of the insulin gene …using ligase which links
together the sugar phosphate backbone of DNA molecule and the plasmid forming RECOMBINANT DNA

Advantages for producing insulin in this way

1. More effective beacuse its identical to human insulin
2. More rapid response.
3. No iummune response
4. Highly pure so no risk of infection being transferred with insulin

5. Cheaper for larger volumes

6. Has fewer ethical and moral objections because animals are not involved in its production
7. Good for people who had developed tolerance to animal insulin
255 / 270
B Growth hormone ..known somatotrophin
Secreted by pituitary gland
Stimulate growth

C Factor VIII …for blood clotting

Factor VIII is called anti hemophiliac factor .

These people with hemophilia ( poor blood clotting due lack of this factor VIII) ….they need regular injection of VIII

In old time they uses donated blood….carry risks for infections

Advantages :
Over coming all problems that can come from blood donations
A) where extracting the factor from blood is difficult as needs many donations to get just small amount of
factor VIII
B) overcoming the risk that factor VIII could be contaminated with disease from donor .
So recombinant DNA technique produce much more factor VIII, more easily and without risk of disease
contamination.
C) over come any ethical objection that people may have to extract and transfer blood / human material
from one person to another .

256 / 270
D Banana vaccine

Vaccine is a very effective way of elimination of diseases

Problem with poor countries , cant afford vaccines
A) required storage in fridge
B) health care workers needed to vaccinate the children

We can use genetically modified plants or plant products such banana , potatoes and carrots
Where they carry vaccines against human disease such as diarrhea or hepatitis B
Advantages
Local communities could grow these modified plants
Which would be relatively cheap and no need for cool storage

257 / 270
 Use of genetically modified plants

1. Extract the Ti plasmid from Agrobacterium

tumefaciens .
2. Insert the gene of interest into the Ti
plasmid using ligase enzyme and insert back
the plasmid ( recombinant DNA) into Transgenic plants
bacterium by heat shock.

3. Infect the plant with the modified bacterium

So that part of the Ti plasmid with the engineered gene become part of the plant plant chromosome.
4. A. tumefaciens Causes tumor to develop on the plant , where these plant cells contain the new gene .
5. Tumor cells are taken and cultured , where a whole new plant can be grown from them ( produce transgenic
plants ).

258 / 270
 Compare bet ween producing a drug from genetically modified plant with that from
genetically modified microorganism .

Drugs from GM plants Drugs from GM microorganisms

Required gene is isolated Required gene is cut from human

from any living organism or any other organism and
and inserted into Ti plasmid inserted into plasmid
of A. Tumefaciens

Plant cells infected by modified Plasmid is transferred into the bacterial host cells where it
bacteria ..transfer the desired gene becomes part of the bacterial DNA ..
to the whole plant genome
Plasmid ….bacteria
Plasmid…..bacteria ….plant

Plant cells are cloned on a suitable media to produce a Transformed bacteria are identifie'd using gene marker …they are
mass of undifferentiated modified plant cells / plant transferred and cultured in fermentors to make the new protein .
cells are grown on a culture to produce new modified
plant cells containing new gene .
-

Plant cells then transferred to suitable Downstream processing required to

medium to produce huge numbers of GM separate the microorganisms and the
plantlets that will mature to produce the desired end product
desired drug in their leaves/fruit etc. 259 / 270
8/ 4/2023
Microarray

260 / 270
Uses of genetical engineering / GM organisms

A . Human

Production of proteins such as insulin, GH , factor VIII

So they are human proteins that dont stimulate an immune response / dont cause allergies

Many people think that the use of GM bacteria in the production of drugs such as
insulin is a very good thing that does not damage the bacteria, but that brings a lot of with
benefit to many people and makes a number of drugs more accessible to people.
Some people think that changing the genetic material of any organisms is interfering
with nature / the will of their God and feel it is unethical and wrong, even if it does
save many lives and improve the quality of life of many people.
against
B. Plants

1. Flood resistant rice .

Jano
2. Plants that are GM to be pest resistance ( inserting a gene that codes for a toxic
substance that kill pests before infecting plants )
3. Modifying plants that are resistant to herbicides . …example Soya beans
Were we use A. Tumefaciens and gene guns to add new gene to soya beans .
4. Changing and increasing nutrients value of plants .
261 / 270
Example soya beans ( GM plants )
A) herbicide resistant to common weed killers
B) fatty acid balance

Normally it contains little oleic acid and stearic acid , large amount of linoleic acid .
Linoleic acid oxidise easily so no longer good for eating

GM soya beans has lots of oleic acid and less linoleic acid …The changed balance of fatty acids in soya beans
benefits the producers because there is a higher percentage of oleic acid. This does not oxidise easily so the soya
beans and their products last longer before going off. This benefits the producers.

Oleic acid is a monounsaturated fatty acid and there is some evidence that it is better for the health than
linoleic acid. So, using products made with the modified soya beans means consumers have potential health
benefits as well as possible price reductions because the beans have a longer shelf life.

C . Animals

Investigate the use of genetically modified animals to produce human medicines …select one
drug and evaluate the success of this process so far

Blood clotting factors such as factor VII and IX from goat / sheep / rabbit milk
Alpha 1 antitrypsin from sheep ( for protection of lungs )
ATryn ( anti thrombin ) ..used in treating hereditary antithrombin deficiency , from goat milk
262 / 270
Evaluation will depend on drug chosen , it should include assessment of cost of producing the drug, effect on animals
used , success of procedure used to creat a transgenic animals , benefits to people who are treated with the drug
compared with previous treatment

Concerns for using genetically modified plants or animals:

1. Animals might give animals an unfair competitive feature over others so cause disruption of food chain .

2. For humans
Open the door to gene manipulation which is ethically un accepted

3. Plants being resistant to herbicides might cross pollinate with a wild relative resulting in the production of super
weeds which are hard to control

4. Might be abused to be used in the production of biological weapons .

5. Only available in certain countries , this lead to discrimination .
6. Strong objections to use animals in scientific research . …unethical

263 / 270
7. Infertile seeds …..as scienetists add marker genes in GM plants ..these marker genes may include
alleles that ensure the plants is infertile so plant cant reproduce
So remove risk of them spreading in the environment
But also this means that farmers must buy fresh supplies of transgenic plant seeds each year for planting
Disadvantage for poor countries ….

8. Antibiotic resistance being used as a gene marker

1. Risk the spreading resistance to other bacteria …
2,. So antibiotics become no longer effective .

9. Risk of eating alien DNA in GM food plants

GM food contains vital medicines or important vitamins …benefit balance shift dramatically
Also there is growing evidence that eating GM food carries no risk and many benefits so in time it would
be no longer of concern. …

264 / 270
Advantages of using plants that have been Disadvantages of using plants that have been genetically
genetically modified modified
1. Cross pollinate with wild relative
1. Tolerant to climate changes such as drought
2. Producing a new more resistant weeds ( super weeds )
resistant .
3. Loss of traditional variety
2. Plants that are GM to be pest resistance so less
4. Loss of genetic diversity
J-4Monoculture.
pesticide used .
5. unknown long term effect of eating GMO / might
3. Modifying plants that are resistant to herbicides . …
have allergic reactions in human so may be unsafe to
example Soya beans reduce competition from weeds
human
4. Changing and increasing nutrients value of plants .
6. Less food available for other animals so affecting rest
5. Flood resistant rice
of food chain
6. Crops can be grown in poor quality land without the
7. GM seed could be difficult to obtain for farmers in
need of fertiliser….gm crops adapted to unfav conditions.
7. Improve food quality . developing countries
8. Cost effective to farmers 8. high cost of buying GM seed …too expensive for
9. Less effect on food chains and pollinators ..so beneficial to farmers to buy as they may have to buy seeds every
environment. season .
10. Produce GM plants that produce vaccine such as GM
9. May not well in all conditions
banana contain vaccine against diarrhea and hepatitis B
10. Under developed countries becoming more dependent
on other countries .

Accumulation of genetically engineered material in the

environment / other species
265 / 270
 Microarrays

D A technique used …….in two ways :

1. Comparing the gene present in complete genomes of two different species ( gene analysis )
2. Finding out which genes are expressed in tissues or cells at any given time ( gene expression profiling)

Is small piece of glass or plastic that has many thousands of tiny spots in known
positions, each spot has many copies of ssDNA with known sequence of bases
Features
1. Thousands of spots are arranged in rows and columns on solid surface of glass , silicon
or plastic .
2. Microarrays can be the size of a microscope slide , or even smaller ( 2 Cm2)
3. Each spot on a microarray contain multiple copies of a single stranded DNS ssDNA.
4. DNA sequence on each spot is unique and known as probe.
5. Each spot represent a single gene or part of a specific gene .
6. The exact location and sequence of each spot is recorded in a computer database ( data
base holding all details about these DNA probes for many genes )

266 / 270
 Using microarray technique to identify genes that are actively transcribed in the……
. Finding out which genes are expressed in tissues or cells at any given time ( gene expression profiling)

1. The mRNA from two types of cells ( diseased and

undiseased ) is extracted and collected …sample
collection and isolation of mRNA
2. And then use reverse transcriptase to use mRNA as
template to produce cDNA
3. Then cDNA is labelled with fluorescent tags
….denatured to give single stranded DNA ……creation
of labelled cDNA
4. and allowed to hybridise with probe on microarray ……
5. each probe is unique to a different gene
6. Spots on the microarray that fluoresce indicate the
genes that were transcribed in the cell ( indicating genes
expressed ) …… ( 4, 5, 6 …hybridisation)
9. The intensity of light emitted by each spot indicate the 7. Collection and anaylsis using bioinformatics/
level of activity of each gene ….high intensity indicates 8. Compare the sequence of the active genes from large
that many mRNA were present in the sample…..and number of individuals with and without disease to
vice versa ( light intensity is proportional to degree of identify mutation
expression) …..thus knowing activity of gene which is
use of bioinformatics / algorithms to analyse the (enormous qua
needed in treating cancer .
of) data (from the microarray) (1) / 267 / 270
Bioinformatics

It’s the development of the software and computing tools that stores , organise and analyses data about the
genomes (DNA sequences) of living organisms.

- Bioinformatics is aiming for :

Facilitate access to large amount of data
Facilitate access to data on DNA and proteins.
Large data base …..where we Use data base to find probes
Fast , accurate ……Using computer soft wares and Statsticl anaylsis

1. When a genome has been sequenced, comparison can be made with other genome …..Compare whole genomes

:
across species to work out evolutionary relationships…. .
2. Also Similarity and comparison can be made between amino acid sequences of proteins or structures of
proteins …close similarities indicate recent ancestors.

3. Compare whole genomes across individuals in one species to find links between genes and diseases…

4- Predict the primary structure of proteins from gene sequences and visulaise the 3D structure ..to identify the
function…so help find a drug that can bind / block the activity / disrupt the structure of protein .

5. To find out when and where genes are expressed during a development .

268 / 270
Mutations in other genes can result in blindness. Describe how these genes could be identified.

1. Using microarray technique to identify genes that are actively transcribed in the eye .
2. . genome of individuals with inherited forms of blindness is sequenced, …..using bioinformatics
3. comparison can be made with other genome …..compare the sequence of active genes from a
large number of individuals with and without blindness to identify mutation .

Steps
1. The mRNA from cells in eye is extracted and collected ( from large number of
individuals with and without blindness ) …sample collection and isolation of mRNA
2. And then use reverse transcriptase to convert mRNA into cDNA …
3. The cDNA is labelled with fluorescent tags ….and allowed to hybridise with
probe ion microarrays ….creation of labeled cDNA
5. Each probe is unique to a different gene .
6. Spots on the microarray that fluoresce indicate the genes that were transcribed
in the cell ( indicating genes expressed ) .. hybridisation
7. Collection and analysis using bioinformatics

269 / 270
 Answered DR. Nihal Gabr
'
(c) Mutations in other genes can result in blindness.
Describe how these genes could be identified.
(3)

Use microarrays technique , to be able to identify genes that are active /

. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

switched on and transcribed in the eye .

. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

The activity of many genes can be anaylsed in a single sample .

. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

Genome of individual with inherited forms of blindness is sequenced .

I
. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

…..compare the sequence of the active genes from a large number of

. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

individuals with and without blindness to identify mutations .

. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

Technique
. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

Sequencing( data base )

. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

Comparison
. . . . . . . . . . . .. .. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ............................................................................................................................................ .............. .. . . . . . . . . . . . . . . . . . . . .

(Total for Question 5 = 10 marks)

Steps
1. The mRNA from cells in eye is extracted and collected ( from large
number of individuals with and without blindness ) …sample collection
and isolation of mRNA
2. And then use reverse transcriptase to produce cDNA using mRNA as
template …
3. The cDNA is labelled with fluorescent tags ….and allowed to hybridise
with probe ion microarrays ….creation of labeled cDNA
5. Each probe is unique to a different gene .
6. Spots on the microarray that fluoresce indicate the genes that were
transcribed in the cell ( indicating genes expressed ) .. hybridisation
7. Collection and analysis using bioinformatics
Genome of the individuals with and without …… is sequenced .
/ Using bioinformatics or data base to analyse the data

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