Physiological Psychology

Module 5
Dr. Navya Pandey
Dr Nesin Mathew
 Module 5
● Hormone and Internal Body States

● Hormones and Behaviour- mechanism of action; Sex hormones: organizing and

activating effects; Puberty.

● Temperature regulation
● Physiological mechanisms of thirst, types of thirst;
● Physiological mechanisms of hunger and satiety.
Hormones and Internal body states
Hormones- Introduction
Secretion of hormones
● Pituitary (ACTH, GH, LH, FSH, PRL, TSH, Oxytocin, ADH)
● Adrenal (Adrenaline, cortisol, Aldosterone)
● Thyroid (Thyroxine)
● Pineal (Melatonin)
● Reproductive glands: ovaries and testes (Testosterone, esterogen, progesterone)
● Pancreas (Insulin, glucagon)
● Hypothalamus (Releasing factors/hormones: for stimulating pituitary; CRH, GnRH,
TRH)
Feedback loop mechanism of hormones
● A feedback mechanism is a loop in which a
product feeds back to control its own
production. Most hormone feedback
mechanisms involve negative feedback loops.
● Negative feedback occurs when a product
feeds back to decrease its own production.
● Eg: Thyroid gland.
● When the level of thyroid hormones is high
enough, the hormones feedback to stop the
hypothalamus from secreting TRH and the
pituitary from secreting TSH.
Feedback loop mechanism of hormones
● Positive feedback occurs when a product feeds back to increase its own production. This
causes conditions to become increasingly extreme.
● An example of positive feedback is milk production by a mother for her baby.
● As the baby suckles, nerve messages from the nipple cause the pituitary gland to secrete
prolactin.
● Prolactin, in turn, stimulates the mammary glands to produce milk, so the baby suckles
more.
● This causes more prolactin to be secreted and more milk to be produced.
● This example is one of the few positive feedback mechanisms in the human body.
Glands can be Exocrine (Which has a duct to release secretion) or
Endocrine (Which secrete directly to blood. No ducts)
Which are the major
endocrine glands in ur our
our body?
3 (in brain) +
7 (in other parts of body)

In addition to this,
Gastrointestinal tract,
Liver, Kidney, heart also
produces hormones
What is the chemical
nature of Hormone
- Amino acid derived,
polypeptides, proteins
and Steroid hormones
derived from
cholesterol
What causes
the secretion of
Hormones?
What are the
stimuli that
leads to
hormone
secretion?
Where does hormones act and how do they act? -
Mechanism of Action

Amplification of stimulus
So very less amount can produce
vast effect in a cell/tissue
Where does hormones act
and how do they act?
Mechanism of Action
Some important notes on hormones
● Single gland- produce multiple hormones Adrenal gland
● Same hormone from many glands-
● One hormone- many receptors- multiple functions
● Hormone synthesis and secretion in periodic manner or cyclic manner
● Same cell can have receptors for many hormones
● A neurotransmitter may also act as hormones
● Glands may have exclusively endocrine function or some can have multiple functions
Hypothalamus and Pituitary
Sex Hormones
● Male hormones: Androgens: Major- Testosterone
● Female hormones: Estrogens: Major Estradiol; Progesterone
● All are steroid hormones containing 4 carbon rings derived from cholesterol
● Steroid hormones such as estrogens and androgens bind to membrane receptors, activate
proteins in the cytoplasm, and activate or inactivate certain genes.
● Estrogens promote typically female features, such as breast development.
● Earlier biologists thought male-female differences are just due to hormones but Later
research demonstrated that some differences depend directly on control by the X and Y
chromosomes independently of hormones (Arnold, 2009).
● So genes on the X and Y chromosomes produce sex differences in addition to those that
we can trace to androgens and estrogens.
Sexual Development
Men and Women
The men-are-men-and-women-are-women assumption is the tendency to think about
femaleness and maleness as discrete,mutually exclusive,opposite categories.
This leads one to assume that females have female sex hormones that give them female
bodies and make them do female things, and that males have male sex hormones that give
them male bodies and make them do opposite male things.

The fact that this approach to hormones and sex is inconsistent with the evidence.
Hormones and behavior
Organizing & Activating effects of sex hormones

● Organizing effects produce long-lasting structural effects.

● The most prominent organizing effects occur during a sensitive stage of early
development—shortly before and after birth in rats and well before birth in
humans—determining whether the body develops female or male anatomy.
● The surge of hormones at puberty also produces long-lasting effects, such as breast
development in women, facial hair in men, and male–female differences in the
anatomy of certain parts of the hypothalamus
● Activating effects are more temporary, when a hormone increases some activity that
lasts only while the hormone is present. Activating effects occur at any time in life.
Organizing effects of sex hormones
● A high level of testosterone causes the external genitals to develop the male pattern, and a
low level leads to the female pattern. (3rd & 4th month of pregnancy)
● Estradiol produces important effects on the internal organs, but it has little effect on the
external genitals.
● Among rats, testosterone begins masculinizing the external genitals during the last several
days of pregnancy and first few days after birth.
● Injecting a genetic male with estrogens produces little effect on his external anatomy.
However, he develops the female-typical pattern of anatomy and behavior if he genetically
lacks androgen receptors, if he is castrated, or if he is exposed to substances that block
testosterone effects.
● Although estradiol does not significantly alter a male’s external anatomy, estradiol and
several related compounds do produce abnormalities of the prostate gland.
● A genetic female that lacks estradiol during the early sensitive period develops
approximately normal female external anatomy but does not develop normal sexual
Organizing Effects of Sex Hormones
● A genetic female that lacks estradiol during the early sensitive period develops
approximately normal female external anatomy but does not develop normal sexual
behavior.
● Even if she is given estradiol injections as an adult, she shows little sexual response toward
either male or female partners
Sex differences in hypothalamus
● Sex hormones early in life influence development in parts of the hypothalamus, amygdala,
and other brain areas
● Eg: One area in the anterior hypothalamus, known as the sexually dimorphic
nucleus, is larger in males than in females and contributes to control of male sexual
behavior.
● Parts of the female hypothalamus generate a cyclic pattern of hormone release, as in the
human menstrual cycle.
● The male hypothalamus cannot, and neither can the hypothalamus of a female who was
exposed to extra testosterone early in life.
Activating effects of sex hormones
● In lower animals, hormonal activation and control of sexual behaviour is usually clear.
● Periodically, when her hormonal status is right, the female will come into heat and be sexually
receptive and attractive to the male.
● In primates, there is no clear relationship between periods of sexual activity and specific phases
of the hormonal cycle.
● Few studies in gorillas and orangutans (Nadler, 1980) do point to mid-cycle peaks of sexual
activity when the female determines sexual interaction. But, as yet, this evidence is limited.
● As far as the human is concerned, many doubt whether hormones play any significant part in
comparison with the powerful effects of social learning.
● The tendency to seek out sexual arousal either by means of imaginary or real behaviour can be
better described as sexual "appetite”
Activating effects of sex hormones
● In the male, who is most likely to initiate sexual interaction, frequency of such activity may be a
function of the level of sexual appetite.
● In the female, this relationship is less apparent. The human male therefore presents a simpler
problem.
● Studies: Androgen replacement in hypogonadal men: Skakkebaek et al. (1981) found
unequivocal effects of androgens in restoring sexual appetite, as reflected in self-ratings of
frequency of sexual thoughts.
● Changes in this measure were the first to occur both with androgen withdrawal and replacement.
● Findings consistent with the above studies were reported in an investigation of the short-term
effects of cyproterone acetate, an anti-androgen, on sexual offenders. Their sexual appetite and
activities reduced post that.
Activating effects of sex hormones
● Few adequately controlled studies of androgen therapy in men with erectile impotence have
produced negative or equivocal results (Bancroft, 1980).
● This is not surprising if, as the studies reported above suggest, erectile mechanisms per se are
relatively independent of androgens.
● On the basis of a number of studies, a small proportion of women show evidence of mid-cycle
peaks, but the majority have no predictable pattern, the major pattern being peaks of sexual
interest or activity before and after menstruation.
● Few recent studies show that the sexual motivation and activity among females increased in the
ovulatory phase (range: day 10-20) which may be th effect of increasing sex hormones just
before, during and just after ovulation.
● But there is little inconsistency in the available research still.
Activating effects of sex hormones
● Several species of whiptail lizard (especially in the genus Aspidoscelis) consist only of females
that have the ability to reproduce through parthenogenesis.
● Females engage in sexual behavior to stimulate ovulation, with their behavior following their
hormonal cycles; during low levels of estrogen, these (female) lizards engage in "masculine"
sexual roles.
● Those animals with currently high estrogen levels assume "feminine" sexual roles. Some
parthenogenetic lizards that perform the courtship ritual have greater fertility than those kept in
isolation due to an increase in hormones triggered by the sexual behaviors.
Hormones regulating Menstrual Cycle
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 Hunger and eating
What triggers hunger?
Why do we eat?
When do we eat?
ow much do we eat?
Why do we stop eating?
 Hunger and eating (theories)
● Digestion: Energy is delivered to body in three forms: lipids, amino acids and glucose
● Energy is stored in three forms: fats, glycogen, proteins
● Preferred way of storing energy??
● Fats store more energy than glycogen. Also glycogen attracts and holds substantial
amt of water
Endocrine glands and hormones
● Pituitary
● Adrenal
● Thyroid
● Pineal
● Reproductive glands
● Pancreas
Endocrine glands and hormones
● Pituitary (ACTH, GH, LH, FSH, PRL, TSH)
● Adrenal (Adrenaline and cortisol)
● Thyroid (Thyroxine)
● Pineal (Melatonin)
● Reproductive glands (Testosterone, esterogen, progesterone)
● Pancreas (Insulin, glucagon)
 Phases of energy metabolism
● Cephalic phase (Preparatory)
● Absorptive phase
● Fasting phase
● Hormones which are important: Insulin, glucagon
● During cephalic and absorptive phase, pancreas releases a lot of insulin
● During fasting phase, insulin is low
 Functions of insulin

● Promotes the use of glucose as the primary source of energy

● Promotes the conversion of bloodborne fuels to forms that can be stored
● Promotes the storage of glycogen in liver, fat in adipose tissue and proteins in muscle
 Phases of energy metabolism
● In contrast to cephalic and absorptive phase, the fasting phase, glucagon level is high
and insulin level is low hence glucose is not the primary fuel for body
● Low level of insulin promotes conversion of glycogen and proteins into glucose
● High levels of glucagon during fasting also promoted the release of free fatty acids
from the adipose tissue and their use as prim fuel
● Also stimulate the conversion of free fatty acids into ketones, which are used by
muscles as a source of energy. After a prolonged fasting, the brain also starts to use
ketones
 Hunger and eating (theories)
● Set-point theories (1940s; 50s)
● Glucostatic set-point theory
● Lipostatic set-point theory
● Based on the concept of homeostasis/negative feedback systems
● Positive incentive theories
 Hunger and eating (theories)
● Limitations of set point theories (food flavour, upbringing; social factors; eating even
not hungry; inconsistent with evolutionary pressure)
● What would an amnesic patient like H.M do if offered a meal shortly after finishing
one?
● How you can relate to the validity of set-point theory?
 Positive incentive perspective
● Positive incentive perspective: humans and other animals are not normally driven to
eat by internal energy deficits but are drawn to eat by the anticipated pleasure of
eating
● Positive incentive value/hedonic value
● It’s not the internal deficit of food but the craving for it because it gives pleasure and
this info is stored in our brain
 Factors influencing what we eat
● Flavour of the food
● What you have learnt about the effects of the food
● The amount of time since you last ate
● The type and quantity of food in your gut
● Whether or not other people are present and eating
● Whether or not blood glucose levels are in normal range
 Factors influencing what we eat
● Species specific pattern of human taste preferences
● Sweet, fatty, salty food (evolutionary perspective)
● Bitter tastes are aversive for humans (adaptive value?)
● Learning of taste preferences and aversions
● Learning of what to eat: Also culturally specific
● Learning to eat vitamins and minerals (experiments with rats etc.)
● Why nutritional deficiencies then?? (because of the hedonistic value of manufactured
foods; also variety of food items available to us)
 Factors influencing when we eat
● Premeal hunger/Meal time hunger: Woods & Ramsay (2000): when the usual
meal time approaches—the body enters the cephalic phase and takes steps to soften
the impact of the impending homeostasis-disturbing influx by releasing insulin into
the blood and thus reducing blood glucose.
● Hunger caused by expectation and not energy deficit
● Pavlovian conditioning of hunger: Weingarten (1983, 1984, 1985): presented rats
with six meals per day at irregular intervals, and he signaled the impending delivery
of each meal with a buzzer-and-light conditional stimulus.
 Factors influencing when we eat
● This conditioning procedure was continued for 11 days.
● Throughout the ensuing test phase of the experiment, the food was continuously
available.
● Despite the fact that the subjects were never deprived during the test phase, the rats
started to eat each time the buzzer and light were presented—even if they had
recently completed a meal.
 Factors influencing how much we eat
● Satiety signals from the gut/blood (glucose; volume of food; nutritive density)
● Sham eating: food is chewed and swallowed by the subject; but rather than passing
down the subject’s esophagus into the stomach, it passes out of the body through an
implanted tube.
● The first sham meal of rats sham eating their usual diet is typically the same size as
previous normal meals, thus indicating that satiety is a function of previous
experience, not the current increases in the body’s energy resources.
 Factors influencing how much we eat
● Appetizer effect and satiety: it occurs because the consumption of small amounts
of food is particularly effective in eliciting cephalic-phase responses.
● Serving size and satiety:
● Social influences:
● Sensory specific: Adult rats that were offered bread and chocolate in addition
to their usual laboratory diet increased their average intake of calories by 84%, and after
120 days they had increased their average body weights by 49%
● As you eat one food, the positive-incentive value of all foods declines slightly, but the
positive-incentive value of that particular food plummets. As a result, you soon
become satiated on that food and stop eating it. However, if another food is offered to
you, you will often begin eating again.
 Factors influencing how much we eat
● (Rolls et al., 1981), human volunteers were asked to rate the palatability of eight
different foods, and then they ate a meal of one of them.
● After the meal, they were asked to rate the palatability of the eight foods once again,
and it was found that their rating of the food they had just eaten had declined
substantially more than had their ratings of the other seven foods.
● Moreover, when the volunteers were offered an unexpected second meal, they
consumed most of it unless it was the same as the first.
 Physiological research
● Role of blood glucose level: Campfield and Smith (1990): the premeal decline
in blood glucose doesn’t produce hunger and eating. Indeed, evidence suggests that
the causation goes in the opposite direction: that the intention to start eating triggers
the decline in blood glucose.
● Hypothalamus hunger and satiety centers: 1950s: Eating behavior is controlled
by 2 centers: Lateral Hypothalamus (LH; feeding); Ventromedial hypothalamus
(VMH; satiety)
● 1940s: Bilateral lesions of VMH caused hyperphagia and obesity in rats
● VMH syndrome: 2 phases: Dynamic: rat overeats after lesions; Static: consumption
gradually declines to maintain a level of obesity
 Reinterpretation of the role of LH & VMH
● LH feeding center: In 1951, Anand & Brobeck bilateral electrolytic lesions :
aphagia (cessation of eating)
● Teitel & Epstein (1962): Aphagia was accompanied by adipsia. LH lesioned rats
partially recover if they are kept alive by tube feeding.
● Reinterpretation: Intial interpretation: VMH lesions rats overeat. New evidence:
they overeat because they become obese. Bilateral VMH lesions increase insulin
levels which increases lipogenesis and decreases lipolysis
● Primary role of the hypothalamus is the energy metabolism and not the regulation of
eating
 Reinterpretation of the role of LH & VMH
● LH lesions: Early research focused exclusively on the aphagia and adipsia that are
produced by LH lesions, but subsequent research has shown that LH lesions produce
a wide range of severe motor disturbances and a general lack of responsiveness to
sensory input (of which food and drink are but two examples).
● Consequently, the idea that the LH is a center specifically dedicated to feeding no
longer warrants serious consideration.
 Role of GI tract in satiety
● Early theory: Cannon & Washburn (1912): Washburn swallowed an empty balloon
tied to the end of a thin tube.
● Cannon pumped some air into the balloon and connected the end of the tube to a
water-filled glass U-tube so that Washburn’s stomach contractions produced a
momentary increase in the level of the water at the other end of the U-tube.
● Washburn reported a “pang” of hunger each time a large stomach contraction was
recorded
● Cannon and Washburn’s finding led to the theory that hunger is the feeling of
contractions caused by an empty stomach, whereas satiety is the feeling of stomach
distention.
 Role of GI tract in satiety
● Support of their theory waned with the discovery of human patients whose stomachs
had been removed: continued to report feelings of hunger and satiety
● Resurgence of interest in the role of GIT in hunger: Koopmans (1981) transplanted an
extra stomach and length of intestine into rats and then joined the major arteries and
veins of the implants to the recipients’ circulatory systems.
● Koopmans found that food injected into the transplanted stomach and kept there by a
noose around the pyloric sphincter decreased eating in proportion to both its caloric
content and volume.
 Hunger and satiety peptides
● New evidence: the stomach and other parts of the gastrointestinal tract release
chemical signals to the brain,
● Ingested food interacts with receptors in the gastrointestinal tract and in so doing
causes the tract to release peptides into the bloodstream.
● In 1973, Gibbs, Young, and Smith injected one of these gut peptides,
cholecystokinin (CCK), into hungry rats and found that they ate smaller meals.
● There has been considerable support for the hypothesis that peptides can function as
satiety signals
● CCK administered to rats after they have eaten an unfamiliar substance induces a
conditioned taste aversion for that substance, and CCK induces nausea in humans.
 Hunger and satiety peptides
● CCK reduces appetite and eating at doses substantially below those required to induce
taste aversion in rats,
● Several hunger peptides (peptides that increase appetite) have also been discovered.
These peptides tend to be synthesized in the brain, particularly in the hypothalamus.
The most widely studied of these are neuropeptide Y, galanin, orexin-A, and ghrelin
● the neural system that controls eating likely reacts to many different signals not just to
one/two
● the discovery that many of the hunger and satiety peptides have receptors in the
hypothalamus has renewed interest in the role of the hypothalamus in hunger and
eating
 Hunger and satiety peptides
● Still it is clear that hypothalamic circuits are only one part of a two-way
communication system between the brain and gut that influences hunger, eating,
digestion, and the regulation of energy resources
● Serotonin and satiety: Blundell & Halford (1998): Serotonin caused the rats to
resist the attraction of highly palatable cafeteria diets
● It reduced the amount of food per meal rather than reducing no of meals
● It was associated with a shift in food preferences away from fatty foods
● Serotonin agonists have been shown to reduce hunger, obesity and body weight in
obese humans
 Prader Willi syndrome
● An accidental chromosomal replication leads to this syndrome in which individuals
experience little or no satiety and an exceptionally slow metabolism
● Other physical and neurological symptoms: weak muscles, small hands and feet,
feeding difficulties during infancy; tantrums, compulsivity; skin picking
● If untreated, patients become obese and die in early adulthood due to diabetes, heart
disease or other obesity related disorders
● Investigation: genetic cause of the condition: an accident of reproduction that deletes
or disrupts a section of chromosome 15 coming from the father.
 Set point vs settling points
● Body fat set point and weight regulation?
● Evidence against it: many people lose or gain large amounts of weights which is
not possible as per the set point theory; Also, the epidemic of obesity due to fast food
eating
● Adult Okinawans (residents of Okinawa island in Japan): consume significantly less
calories than advised by health officials but are relatively healthy and mortality rate
and aging related diseases are low in their society..
● Some evidence suggests that dietary restriction/calorie restriction can have beneficial
effects on the health and longevity (various studies)
● Caloric restriction has been shown to reduce seizure susceptibility in human
epileptics and to improve memory among elderly
 Set point vs settling points
● Diet induced thermogenesis: The mechanism by which the body adjusts the
efficiency of its energy utilization in response to its body fat levels
● Increases in the levels of body fat produce increases in body temperature, which
require additional energy to maintain them—and decreases in the level of body fat
have the opposite effects
● Settling-point model: body weight tends to drift around a natural settling point—the
level at which the various factors that influence body weight achieve an equilibrium.
● The idea is that as body-fat levels increase, changes occur that tend to limit further
increases until a balance is achieved between all factors that encourage weight gain
and all those that discourage it.
 Set point vs settling points
● According to the settling-point model, body weight remains stable as long as there are
no long-term changes in the factors that influence it; and if there are such changes,
their impact is limited by negative feedback.
● In the settling-point model, the negative feedback merely limits further changes in the
same direction, whereas in the set-point model, negative feedback triggers a return to
the set point.
Thirst
 Thirst
● Approximately two thirds of the body’s
water is contained in the intracellular fluid
(67%)

● The rest is extracellular fluid

(intravascular/blood plasma:7 %,
interstitial 26%, CSF: less than 1 %)
 Thirst
Two types of thirst:
● Osmotic thirst (Eating salty foods):
● Hypovolemic thirst (losing fluid)
● Osmotic thirst: Osmotic pressure is the tendency of water to flow across a
semipermeable membrane from the area of low solute concentration to the area of
higher concentration.
● If you eat something salty, sodium ions spread through the blood but the extracellular
fluid do not cross the membranes into cells.
● The result is a higher concentration of solutes (including sodium) outside the cells
than inside.
 Thirst
● The resulting osmotic pressure draws water from the cells into the extracellular fluid.

● Certain neurons detect their own loss of water and then trigger osmotic thirst, which helps
restore the normal state

● Extracellular fluid hyperosmolality stimulates the sensation of thirst to promote water

intake and the release of vasopressin that will enhance water reabsorption in the kidney.
The kidneys also excrete extra sodium through concentrated urine and maintain as much
water as possible

● By contrast, extracellular fluid hypo-osmolality suppresses basal vasopressin secretion.

 Brain areas controlling osmotic thirst
● Receptors around the third ventricles
● Weak blood brain barrier in that area; helps in monitoring the contents of the blood
● The areas important for detecting osmotic pressure and the salt content of the blood
include the OVLT (organum vasculosum laminae terminalis) and the subfornical
organ (SFO)
● Receptors in the OVLT, the subfornical organ, the stomach, and elsewhere relay their
information to several parts of the hypothalamus, including the supraoptic nucleus
and the paraventricular nucleus (PVN), which control the rate at which the
posterior pituitary releases vasopressin.
 Brain areas controlling osmotic thirst
● It is also thought that these SFO and OVLT neurons monitor the blood osmolality
directly, possibly via stretch-sensitive ion channels embedded in their plasma
membranes that detect changes in cell volume following intracellular dehydration
 Thirst
● Stop drinking: The water you drink has to be absorbed through the digestive system
and then pumped through the blood to the brain.
● That process takes 15 minutes or so, and if you continued drinking for that long, you
would drink far more than you need.
● The body monitors swallowing and detects the distension of the stomach and upper
part of the small intestine.
● Those messages limit drinking to not much more than you need at a given time
 Hypovolemic Thirst
● Hypovolemic/sodium specific hunger (losing fluid by
sweating/bleeding/vomiting/diarrhea):
● When blood volume drops, the kidneys release the enzyme renin, which splits a
portion off angiotensinogen, a large protein in the blood, to form angiotensin I,
which other enzymes convert to angiotensin II.
● Like vasopressin, angiotensin II constricts the blood vessels, compensating for the
drop in blood pressure
● Angiotensin II also helps trigger thirst, in conjunction with receptors that detect blood
pressure in the large veins.
● However, this thirst is different from osmotic thirst, because you need to restore lost
salts and not just water. This kind of thirst is known as hypovolemic thirst
 Hypovolemic Thirst
● When angiotensin II reaches the brain, it stimulates neurons in areas adjoining the
third ventricle
● Those neurons send axons to the hypothalamus, where they release angiotensin II as
their neurotransmitter
● the neurons surrounding the third ventricle both respond to angiotensin II and release
it.
● Whereas an animal with osmotic thirst needs water, one with hypovolemic thirst can’t
drink much pure water.
● If an animal is offered both water and salt, it alternates between them to yield an
appropriate mixture. It shows a strong craving for salty tastes.
 Hypovolemic Thirst

● This preference is known as sodium-specific hunger which develops automatically as

soon as the need exists
● When the body’s sodium reserves are low, the adrenal glands produce the hormone
aldosterone which causes the kidneys, salivary glands, and sweat glands to retain
salt
● Aldosterone and angiotensin II together change the properties of taste receptors on
the tongue, and neurons elsewhere in the brain to increase salt intake
●
 Hypovolemic Thirst
● Aldosterone indicates low sodium and angiotensin II indicates low blood volume.
● Either one by itself produces only a small effect on salt intake, but their combined
effect is a massive increase in a preference for salt, sometimes producing a preference
for salt over sugar or anything else
●
Temperature regulation
 Temperature regulation
● Homeostasis: temperature regulation and other biological processes that keep body
variables within a fixed range.
● Set point and negative feedback
● Allostasis:the adaptive way in which the body changes its set points depending on
the situation
● Many animals increase their body fat in fall and decrease it in spring.
● The body maintains a higher temperature during the day than at night, even if room
temperature stays constant.
 Temperature regulation examples
Temperature affects behavior in many ways
● Gulls, ducks, or other large birds standing on one leg
● Vultures sometimes defecate onto their own legs.
● Toucans are tropical birds with huge bills
● Most lizards live solitary lives, but Australian thick-tailed geckos sometimes form
tight huddles.
● Migratory birds do most of their migratory flying at night.
 Controlling body temperature
● Basal metabolism: We use a lot of energy in basal metabolism (the energy used to
maintain a constant body temperature while at rest).
● Poikilothermic animals: Amphibians, reptiles; A desert lizard moves between sunny
areas, shady areas, and burrows to maintain a fairly steady body temperature. However,
behavioral methods do not enable animals to maintain the same degree of constancy that
mammals and birds have.
● Homeothermic animals/Endotherms/warm-blooded: Mammals: 37 degree celsius or
98 degree fahrenheit
● Homeothermic animals use physiological mechanisms to maintain a nearly constant body
temperature despite changes in the temperature of the environment.
 Controlling body temperature
● Humans sweat to expose water for evaporation. For species that don’t sweat, the
alternatives are licking themselves and panting. As water evaporates, it cools the body.
● Several physiological mechanisms increase your body heat in a cold environment.
● One is shivering. Any muscle contractions, such as those of shivering, generate heat.
● Second, decreased blood flow to the skin prevents the blood from cooling too much.
● We also use behavioral mechanisms, just as poikilothermic animals do. In fact, we prefer
to rely on behavior when we can.
 Brain mechanism
● The physiological changes that defend body temperature—such as shivering,
sweating, and changes in blood flow to the skin—depend on areas in and near the
hypothalamus mainly the anterior hypothalamus and the preoptic area,
● The POA/AH monitors body temperature partly by monitoring its own temperature
(D. O. Nelson & Prosser, 1981).
● If an experimenter heats the POA/AH, an animal pants or sweats, even in a cool
environment. If the same brain area is cooled, the animal shivers, even in a warm
room.
● Cells of the POA/AH also receive input from temperature receptors in the skin and
spinal cord. The animal shivers most vigorously when both the POA/AH and the
other receptors are cold. It sweats or pants most vigorously when both are hot.
 Brain mechanism
● Separate populations of cells within the POA/AH and a couple other hypothalamic
areas regulate different aspects of temperature regulation, such as shivering and
changes in blood flow.
● Therefore, tiny localized damage can impair one aspect of temperature regulation and
not others
● After damage to all of the POA/AH, mammals can still regulate body temperature but
only by the same behavioral mechanisms that a lizard might use,
 Fever
● When bacteria, viruses, fungi, or other intruders invade the body, they mobilize
leukocytes (white blood cells) to attack them. The leukocytes release small proteins
called cytokines that attack the intruders.
● Cytokines also stimulate the vagus nerve, which sends signals to the hypo-
● thalamus (Ek et al., 2001; Leon, 2002), increasing the release of chemicals called
prostaglandins.
● Stimulation of a particular kind of prostaglandin receptor in one nucleus of the
hypothalamus is necessary for fever.
● Genetic mutations can hamper this ability (cases not having prostaglandin rec)
● A fever represents an increased set point for body temperature.
 Fever
● When you have a fever, you shiver or sweat whenever your temperature deviates
from that level.
● Newborn rabbits have an immature hypothalamus, they do not shiver in response to
infections. If they are given a choice of environments, however, they select a spot
warm enough to raise their body temperature. That is, they develop a fever by
behavioral means.
● Fever is just an indicator of infection in body
● Other benefit: Certain types of bacteria grow less vigorously at high temperatures
● It also enhances activity of the immune system
● A fever above about 39° C (103° F) in humans does more harm than good, and a
fever above 41° C (109° F) is life-threatening