This document provides an overview of hormones, including: 1. Hormones are chemicals secreted by endocrine glands that travel through the blood and influence other glands and organs. There are two major classes: protein hormones and steroid hormones. 2. The hypothalamus and pituitary gland control hormone release through negative feedback loops. The hypothalamus secretes hormones that stimulate or inhibit the pituitary gland. 3. Hormone disorders can occur if glands do not produce the proper hormones. Examples include congenital adrenal hyperplasia and androgen insensitivity syndrome.

1. 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. 5α- Reductase Deficiency.
• This is a deficiency of the enzyme 5α-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.