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Action Potentials and Synaptic Transmission

The document explains the concepts of resting potential, action potential, and synaptic transmission in neurons. It details the mechanisms of depolarization and repolarization during action potentials, the role of neurotransmitters like acetylcholine, and the processes of excitatory and inhibitory postsynaptic potentials. Additionally, it covers the refractory periods and the coding of stimulus intensity through action potentials.

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0% found this document useful (0 votes)
5 views23 pages

Action Potentials and Synaptic Transmission

The document explains the concepts of resting potential, action potential, and synaptic transmission in neurons. It details the mechanisms of depolarization and repolarization during action potentials, the role of neurotransmitters like acetylcholine, and the processes of excitatory and inhibitory postsynaptic potentials. Additionally, it covers the refractory periods and the coding of stimulus intensity through action potentials.

Uploaded by

reeves120502
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Resting Potential RP = -70mv

Action Potential AP = +30 mv


Resting Potential

At rest, all cells have a negative internal charge and


unequal distribution of ions:Results from:
Large cations being trapped inside cell
Na+/K+ pump and limited permeability keep Na+ high outside cell
K+ is very permeable and is high inside cell
Attracted by negative charges inside
Explained by Nernst Equation p. 149

7-27
Membrane Potential (MP) Changes
• Measured by placing 1
electrode inside cell and
1 outside
• Depolarization occurs
when MP becomes more
positive
• Hyperpolarization: MP
becomes more negative
than RMP
• Repolarization: MP
returns to RMP
7-29
The Action Potential (AP)
• Is a wave of MP change that sweeps along the
axon from soma to synapse
• Wave is formed by rapid depolarization of the
membrane by Na+ influx; followed by rapid
repolarization by K+ efflux

7-33
Mechanism of Action Potential
• Depolarization:
– At threshold, VG Na+ channels open
– Na+ driven inward by its electrochemical gradient
– This adds to depolarization, opens more channels
• Termed a positive feedback loop
– Causes a rapid change in MP from –70 to +30 mV

7-34
Mechanism of Action Potential continued
• Repolarization:
– VG Na+ channels close; VG K+ channels open
– Electrochemical gradient drives K+ outward
– Repolarizes axon back to RMP

7-35
Mechanism
of Action
Potential
continued

7-37
APs Are All-or-None
• When MP reaches
threshold an AP is
irreversibly fired
– Because positive
feedback opens
more and more
Na+ channels
– Shortly after
opening, Na+
channels close
• and become
inactivated until
repolarization
7-38
How Stimulus Intensity is Coded
• Increased stimulus intensity causes more APs to be fired
– Size of APs remains constant

7-39
Refractory Periods
• Absolute refractory
period:
– Membrane cannot
produce another AP
because Na+
channels are
inactivated
• Relative refractory
period occurs when
VG K+ channels are
open, making it
harder to depolarize
7-40
Synapse

• Is a functional connection between a neuron


(presynaptic) and another cell (postsynaptic)
• There are chemical and electrical synapses
– Synaptic transmission at chemical synapses is via
neurotransmitters (NT)
– Electrical synapses are rare in NS

7-47
Chemical Synapse

7-49
Synaptic Transmission continued

• NT (ligand) diffuses across cleft


– Binds to receptor proteins on postsynaptic
membrane
• Opening chemically-regulated ion channels
– Depolarizing channels cause EPSPs (excitatory
postsynaptic potentials)
– Hyperpolarizing channels cause IPSPs (inhibitory
postsynaptic potentials)
– These affect VG channels in postsynaptic cell

7-52
Synaptic Transmission continued

7-54
Acetylcholine (ACh)

• Most widely used NT


– Used in brain and ANS; used at all neuromuscular
junctions
• Has nicotinic and muscarinic receptor subtypes
– These can be excitatory or inhibitory

7-55
Acetylcholine in the PNS
• Cholinergic neurons use acetylcholine as NT

• The large synapses on skeletal muscle are


termed end plates or neuromuscular junctions
(NMJ) = Myoneuronal Junction
– Produce large EPSPs called end-plate potentials for
muscles; causing muscle contraction

– Curare blocks ACh action at neuromuscular


junctions by occupying ACh receptors; causing
relaxed muscles (used to assist surgery )

7-62
Acetylcholinesterase (AChE)
• Inactivates ACh, terminating its action; located in cleft

7-60
Nicotinic ACh Channel

– Permits diffusion of Na+ into


and K+ out of postsynaptic cell

– Inward flow of Na+ dominates

– Produces EPSPs in skeletal


muscle

7-57
Muscarinic ACh Channel

• Binding of 1 ACh activates G-protein cascade


which affects gated K+ channels
– Opens some, causing hyperpolarization (ex.
Slows SA-node Heart pacemaker)

– Closes others, causing depolarization

7-59
Monoamine Neurotransmitter 2nd messenger
action

2nd Messenger = cyclic AMP


7-65
EPSPs
• Graded in magnitude
• Have no threshold

• Cause depolarization
• Summate

• Have no refractory period

7-76
Temporal Summation
• Temporal summation occurs because EPSPs that occur
closely in time can sum before they fade. At same location
close together in time.

7-78
Spatial Summation

• Cable properties cause


EPSPs to fade quickly
over time and distance

• Spatial summation takes


place when EPSPs from
different synapses occur
in postsynaptic cell at
same time. At same time
close together in location.
7-77

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