This document provides an overview of hormones and their functions. It describes hormones as chemicals secreted by endocrine glands that influence other glands and organs. There are two major classes of hormones - protein hormones like insulin and glucagon, and steroid hormones derived from cholesterol like corticoids and sex steroids. The release of hormones is controlled by the hypothalamus and pituitary gland using negative feedback systems. Specific hormonal disorders that impact sexual development and characteristics are also discussed, as well as the effects of pheromones on behavior in animals and humans.

1. Biological Bases of Behaviour.
Lecture 6: Hormones.

2. Learning Outcomes.
• By the end of this lecture you should be able to:
• 1. Describe the different types of hormones and their key
actions.
• 2. Explain the neural control of hormone release.
• 3. Describe specific hormonal disorders.
• 4. Explain the term 'pheromone' and provide examples of
pheromones in action.

3. What Are Hormones?
• Hormones are chemicals secreted by endocrine glands

4. How Do Hormones Work?
• Hormones travel through the blood and influence the
activity of other glands and organs.
• They produce short- and long-term changes in various cells
and organs by acting like neurotransmitters at
metabotropic receptors.
• A hormone can only influence cells that have specific target
receptors for that particular hormone.

5. Types of Hormones.
• Endocrine glands produce 2 major classes of hormones
(and several other types as well):
• 1. Protein hormones: These comprise amino acids, those
that are only several amino acids in length are called
peptide hormones, whereas larger ones are called
polypeptide hormones. They include:
• Insulin: Made in the pancreas, it increases the entry of
glucose into the cells, and regulates fat storage.
• Glucagons: Made in the pancreas, are responsible for
increasing the conversion of stored fats to blood glucose.
• Leptin: Produced by the fat cells, it informs the brain how
much fat is contained in the body.

6. Leptin in Action.
 When leptin levels are high
appetite is decreased.
 When leptin levels are low
appetite is increased and
bodily activity is reduced.
 Mice who inherit 2 copies of
the defective ob gene are
unable to produce leptin
and so overeat.
 Injections of leptin reduce
their food intake.

7. 2. Steroid Hormones.
• These are derived from cholesterol from the diet and exert
their effects in two ways:
• i) They bind directly to membrane receptors.
• ii) As they are fat soluble they pass through cell
membranes where they attach to receptors in the
cytoplasm. Here they determine gene expression.
• There are several types of steroid hormones:
• a) Corticoids.
• Glucocorticoids (principally cortisol) are released by the
adrenal glands in response to stress.
• They increase the breakdown of fats and proteins into
glucose to trigger escape or defense ("fight or flight").
• Mineralocorticoids (e.g. aldosterone) are also produced by
the adrenal glands and reduce salt secretion in the kidneys.

8. b) Sex Steroids.
• These are released mainly by the ovaries and testes but
also by the adrenal glands. They comprise:
• Androgens: Testosterone is produced in large amounts in
males and has masculinising and defeminising effects;
maintaining male secondary sexual characteristics and
promoting courtship, aggressive and sexual behaviours.
• Estrogens: Estradiol is produced in large amounts in
females and has feminising effects, promoting female
secondary sexual characteristics, water retention, calcium
metabolism, sexual behaviour and maternal behaviours.
• Progesterone prepares the uterus for the implantation of a
fertilised ovum and regulates the stages of pregnancy.

9. Misunderstandings.
• According to Nelson (2000), there are several
misunderstandings surrounding hormones:
• 1. Sex steroids are sex-specific: In fact both males and
females produce androgens and estrogens though their
relative concentrations differ.
• 2. Individual differences in behaviour and physiology
reflect differences in hormone concentration: While overall
concentration is indeed important, of equal importance is
the receptivity of the cells to the hormone.
• A high hormone concentration will have little effect if cells
lack receptivity, an excellent example of this is Androgen
Insensitivity Syndrome.

10. Control of Hormone Release.
• Hormone release is controlled by two key structures in the
brain:
• 1. Hypothalamus: This is located at the base of the brain
and consists of several interconnected nuclei.
• The hypothalamic nuclei synthesise releasing hormones
that either stimulate or inhibit the release of hormones
from the pituitary gland.
• The hypothalamus also secretes oxytocin and vasopressin
which travel to the posterior pituitary gland. This then
releases them into the bloodstream in response to certain
neural signals.

11. Negative Feedback in the
Hypothalamus.
• The hypothalamus maintains fairly constant levels of
hormones because it operates a negative feedback system.
E.g:
Hypothalamus
Thyroid Stimulating Hormone-
Releasing Hormone
Anterior pituitary
Thyroid gland
Thyroid Stimulating Hormone
Thyroid
hormones
excitatory
inhibitory

12. 2. Pituitary Gland.
• This is called ‘the
master gland’ as it
produces at least 10
hormones which
influence the other
endocrine glands via
the hypothalamus.
• It consists of two
separate regions.
• The anterior pituitary
and the posterior
pituitary each share
distinct connections
with the
hypothalamus.
hypothalamus
Posterior
pituitary
Vasopressin
and oxytocin
GH, ACTH,
TSH, FSH, LH
and prolactin
Anterior
pituitary
Blood
supply

13. Anterior Pituitary Gland.
• Hormones produced here are referred to as tropic as they
stimulate various processes:
• Luteinizing Hormone (LH): Increases production of
progesterone and stimulates ovulation in females. In males
it increases production of testosterone.
• Follicle-Stimulating Hormone (FSH): Increases production
of estrogen and maturation of the ovum (in females) and
sperm (in males).
• Thyroid-Stimulating Hormone (TSH): Controls secretions of
the thyroid gland.
• Growth Hormone (GH): Increases body growth.
• Prolactin: Controls milk production in females.
• Adrenocorticotropic Hormone (ACTH): Controls secretions
of the adrenal gland.

14. Posterior Pituitary Gland.
 This stores oxytocin which controls uterine contractions,
milk release, parental behaviours and orgasm.
 It also stores vasopressin (also known as antidiuretic
hormone) which constricts blood vessels, raises blood
pressure, and decreases urine volume.

15. Hormones and Behaviour.
• Hormones do not cause a particular behaviour to change,
rather they change the likelihood that a particular
behaviour will occur in an appropriate environmental
context.
• Certain behaviours can also influence hormone levels, e.g.
testosterone levels can rise or fall depending upon whether
a contest has been won or lost.
• This is a ‘chicken and egg’ problem, i.e. do hormones
influence behaviour by directly affecting the brain, or does
behaving in a particular manner influence hormone
production?
• In order to decide we can use three techniques:

16. Experiments to Test
Hormone/Behaviour Relationships.
• 1. If we remove the source of a particular hormone then a
behaviour that is assumed to depend upon that hormone
should disappear. E.g removal of testosterone by castration
dramatically reduces sexual desire and aggression in many
male animals.
• 2. Once a behaviour has ceased following hormone
removal, we can restore hormone function and see if the
behaviour returns. E.g administration of testosterone to
castrated adult males restores aggressive behaviours and
the mating urge.
• 3. If hormones and certain behaviours are related, then we
should expect that alterations in the relative concentration
of a hormone should produce related alterations in a
behaviour. E.g aggression should be higher when
circulating levels of testosterone are higher.

17. Human Hormone Disorders.
• 1. Congenital Adrenal Hyperplasia (CAH).
• This is a genetic disorder producing enzyme deficiency in
the adrenal glands.
• The glands are unable to produce sufficient quantities of
cortisol which normally inhibits the release of
adrenocorticotropic hormone (ACTH) which promotes sex-
steroid synthesis.
• ACTH is thus produced in large amounts and the foetus is
exposed to excessive amounts of androgens which have a
masculinising effect.
• Affected females display masculinised genitals and
behaviour. Affected males may show precocious puberty.

18. 2. Androgen-Insensitivity Syndrome
(AIS).
• An X-linked recessive disorder
(affecting only males) in which
androgen receptors in the cells do
not function.
• The male brain and body remain
unresponsive to androgens and
are feminised due to maternal
estrogens.
• At puberty the testes do not
descend and secondary female
sexual characteristics appear due
to circulating estrogens.
• Individuals are often reared as
girls and do not discover that they
are ‘male’ until they fail to
menstruate at puberty.

19. 3. Idiopathic Hypogonadotropic
Hypogonadism (IHH):
• This is caused by the insufficient release of gonadotropin
releasing hormone from the hypothalamus.
• It is sometimes referred to as ‘Kallman’s Syndrome’.
• Affected males are genetically normal, but do not receive
sufficient testosterone before birth.
• Their genitals remain relatively unaffected due to the
influence of maternal androgens, but at puberty secondary
male sex characteristics fail to appear.

20. 4. Turner’s Syndrome.
• This syndrome was first described by Turner (1938).
• It only affects females in which all or part of one X
chromosome is deleted.
• This leads to a failure in ovary development, and produces
short stature and physical anomalies such as webbing of
the neck.
• Externally, such individuals appear female but as they fail
to produce female sex hormones they remain sexually
immature unless provided with hormone replacements.
• They remain infertile.

21. 4. 5- Reductase Deficiency.
• This is a deficiency of the enzyme 5-reductase which
normally converts testosterone into dihydrotestosterone.
• As dihydrotestosterone is principally responsible for
masculinising the external genitals before birth, males with
this syndrome are born with ambiguous genitalia and
undescended testes.
• They are often mistaken for females at birth and reared as
such.
• However at puberty when exposed to large amounts of
testosterone their body and external genitals become more
masculine.

22. Pheromones.
• These are chemicals derived from sex hormones which are
manufactured and released by the apocrine glands.
• They are released into the environment via sweat and urine
where they are detected by individuals of the same species in
whom they activate specific physiological and behavioural
responses.
• The following effects have been noted in animals:

23. Pheromone Effects in Animals.
 Lee-Boot effect: When groups of female mice are housed
together their estrus cycles slow down and stop.
 Whitten effect: If groups of female mice are then exposed
to an adult male mouse (or to the odour of his urine) they
begin estrus again and their cycles become synchronised.
 Similar menstrual synchrony has been reported in human
females sharing accommodation.
 Vandenburg effect: The presence of an unrelated adult
male causes the acceleration of puberty in female rats. This
has also been reported for human females in the presence
of a stepfather.
 Bruce effect: When a pregnant female mouse is housed
with a male mouse who is not the father the pregnancy is
likely to fail and she quickly comes into estrus again.

24. Effects of Human Pheromones.
• At puberty, pheromones derived from androgens act as
sexual attractants. E.g. Thorne et al., (2002) found that non-
pill using females unknowingly exposed to male pheromones
gave higher attractiveness ratings to photographs of males
faces.