Sexual differentiation and sex differences in behaviour. Flashcards
1
Q
What is sexual differentiation?
A
Developmental process of becoming male or female
2
Q
Explain the process of sexual differentiation
A
- Primary step occurs at fertilisation when chromosomal make up is determined (this is called sex determination)
- Sexual differentiation is complicated and the potential for atypical development is high
3
Q
What does chromosomal sex mean?
A
XX (female)
XY(male)
determined gonadal sex, so the ovaries or testes.
4
Q
What is morphological sex?
A
Body type, e..g if you physically look male or female because of external genetalia
5
Q
What is** hormonal sex?**
A
refers to an individual’s sex as determined by their hormonal profile. e.g steroid hormone concentrations like testosterone or estrogen
6
Q
What is behavioural sex?
A
Can be interpreted as referring to behaviors that are typically associated with a particular sex or gender. These behaviors can encompass a wide range of actions, interests, and social roles that are culturally or biologically influenced and are often associated with masculinity or femininity.
7
Q
Tell me the **characteristics **and incidience of a **XYY **chromosomal makeup?
A
8
Q
Tell me the characteristics and incidience of a **XYY **chromosomal makeup?
A
- Male
- Tall
- Learning difficulties
- Incidence : 1/1000 male births
9
Q
Tell me the **characteristics **and incidience of a **XXX (Triple X) **chromosomal makeup?
A
- Female
- Tall
- Learning Difficulties
- Incidence : 1/1000 female births
10
Q
Tell me the **characteristics **and incidience of a **XXY (Klinefelter) **chromosomal makeup?
A
- Male
- Infertile
- Incidence : 1/1000 male births
11
Q
Tell me the **characteristics **and incidience of a **XO (Turner) **chromosomal makeup?
A
- Female
- Short
- Infertile
- Skeletal and organ abnormalities
- Incidence : 1/3500 female births
12
Q
How and when do Gonads develop?
A
- 6-7 weeks of development
- Thickened ridge of tissue on protokidney (germinal ridge) starts to develop in to gonads
- the default direction is female, the germinal ridge becomes an ovary if there are no signals from the SRY gene located on the Y chromosome. This gene produces TDF which forms testes and then the development continues in a male direction.
13
Q
Explain how male development starts?
A
- 6-7 weeks of development
- SRY (Sex-determining Region on the Y chromosome) gene activates which is located on the Y chromosome.
- This starts producing TDF (testis determining factor; a protein)
- The germinal ridge then turns into testes not ovaries.
14
Q
When could an XX individual develop testes?
A
If the SRY gene is transposed on a X chromosome, XX individuals will then develop testes and male genetalia (1/20,00 births)
15
Q
What is Swyer syndrome?
A
Swyer syndrome is where the SRY gene has mutated. Meaning, instead of testes or ovaries developing, something called ** ‘streak gonads’** develop, this is non functional tissue. Meaning those with this syndrome will have to have hormonal replacement therapy to go through puberty.
16
Q
What is the Mullerian duct system?
A
**Female accessory sex organ **- develops into fallopian tubes, uterus and cervix
Until 6 weeks, embryos have BOTH Mullerian and Wolffian
17
Q
What is the Wolfian duct system?
A
Male accessory sex organ, develops into vas deferns, seminal vesicle.
Until 6 weeks, embryos have BOTH Mullerian and Wolffian
18
Q
Tell me what promotes development in a male direction?
A
Androgens ! these promote development in a male direction (testosterone)
19
Q
Tell me what promotes development in a female development?
A
The absence of androgens, ovaries do not produce high concentrations of hormones therefore the absence of androgens promoted development in a female direction.
20
Q
What are ANDROGENS?
A
Group of hormones testosterone,androstenedione,dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEA-S)
21
Q
What are the 3 peaks in androgen production?
A
- 10-18 weeks of pregnancy (differentiation of reproductive system)
- 2-6 months after birth
- Puberty (secondary sexual characteritics)
22
Q
What does Testosterone do?
A
Determines male sexual characteristics
1. Libido
2. Bone formation
3. Metabolism
4. Red Blood cell formation
5. Mood, confidence
6. Memory function
23
Q
What is Testosterone synthesis in males?
A
Occurs within the testes, within specialised cells called LEYDIG cells.
These cells produce 96% of Testosterone in the male body from Cholesterol
The remaining 5% are produced in the Adrenal Glands
24
Q
What is Testosterone synthesis in females?
A
-
Testoserone is produced by the ovaries and varies across the menstrual cycle :
50% from ovaries
50% from adrenal glands - Adult female testosterone levels are approx 1/10th of male levels.
- The enzyme aromatase converts testosterone into estradiol through the process of aromatisation. Estradiol is a type of estrogen, this is the primary hormones responsible for female characteristics and sexual functioning.
25
What does the **enzyme aromatase** do?
It converts testosterone into estardiol through a process called aromatisation
25
What is **aromatisation**?
Aromatisation is the process that turns helps the enzyme aromatase turn testosterone into estradiol.
26
What is **estradiol** and what is it responsible for?
A type of **estrogen**, that the enzyme aromatase converts testosterone into.
Primary hormone responsible for female characteristics and sexual functioning.
27
What are the **female sex** hormones?
**Estrogens**
- Estrone (E1)
- Estradiol (E2)
- Estriol (E3)
28
What are the role of **Estrogens**
Control the development and maintenance of female sexual characteristics. Involved in cholesterol regulation, bone/heart/skin health and mood.
29
What is **Estrone (E1)** ?
The only type of estrogen found in women **after menopause**, small amounts of estrone are present in most tissues of the body, mainly fat and muscle.
30
What is **Estradiol (E2)**?
A **steroid **produced from testosterone by the gonads
31
What is **Estriol (E3)**
**A waste product of Estradiol**. significant amounts are made during pregnancy.
32
What is the role of **Progesterone**?
Linked to the menstrual cycle, pregnancy, adn the development of an embryo. Also, involved in bone health, hair growth, metabolism, mood.
33
Where are **estrogens** and **progesterone** produced?
| 3 places
1. Ovaries (corpus luteum)
2. Adrenal glands
3. Placenta
34
What **3** places do men produce **estrogens** and **progesterone**?
produced from cholestrol
1.testes
2. bones
3. adipose tissue - body fat
35
Do **estrogens in men **act :
A- locally
or
B - further away ?
**A!**
They act locally, which limits their systemic effects
36
What is GnRH?
**Gonadoptropin-releasing-hormone**
Secreted from the hypothalamus it determines the pattern of release of gondotropins (hormones that act on the gonads) from anterior pituitary gland.
37
What is **LH**?
**Luteinizing Hormone** - stimulate ovaries and testes
38
What is **FSH** ?
**Follicle-stimulating-hormone**-
stimulates ovaries and testes
39
How is **testosterone regulated**?
Through a **negative** feedback loop
40
Explain the **negative feedback** loop of **testosterone**
| control of sex hormones in males
1. Begins in hypothalamus, releases GnRH (onadotropin-Releasing Hormone) in signals.
2. GnRH stimulates the pituitary gland, this releases LH and FSH , LH plays a key role in regulating testosterone production.
3. LH travels to the testes via blood, bind to receptors on specialised Leydig cells. Leydig cells are responsibe for producing testosterone in response to LH stimulation.
4. The Leydig cells then synthesise (make) and release testosterone.
5. As testosterone rises in the blood, this exerts a negative feedback on the hypothalamus and pituitary gland to regulate further hormone production. HIgh levels of T signals to the hypothalamus to decrease the release of GnRH, which then reduces LH secretion by the pituitary glands.
6. With less LH to stimulate the Leydig cells, testosterone synthesis (production) decreases.
41
Explain the **control of sex hormones** in females
| negative and positive feedback loop
1. Hypothalamus releases GnRH because of signals (hormonal or environmental)
2. GnRH stimulates pituitary gland, which stimulates production of LH and FSH
3. LH and FSH travel via blood to ovaries, stimulating the production and release of estrogen and progesterone by ovarian follicles.
4. During follicular stage (12-14 days of cycle), FSH stimulates the growth and development of ovarian follicles, releasing estrogen.
5. Negative feedback loop - as estrogen levels rise, this exerts negative feedback on the hypothalamus and pituitary, inhibiting GnRH, LH and FSh - regulating the timing of the menstrual cycle.
6. Following ovulation, the ruptured follicle transforms into a structure called the corpus luteum (temporary gland where egg used to be), this produces progesterone. The progesterone along with estrogen helps prepare the uterine lining for possible implantation of a fertilised egg.
7. If fertilisation and implantation does not occur, estrogen and progesterone levels delcine which causes the sheeding of the uterine lining (menstruation) decline in hormone levels relieves the negative feedback on the hypothalamus and pituitary gland- allowing GnRH, LH and FSH inititaing a new menstrual cycle.
42
What is an example of **positive feedback** loop in the **female cycle**?
**Ovulation**
- as ovarian follicles mature, estrogen rises - this triggers LH to be released from pituitary
- LH releases the mature egg from follicle - initiating ovulation.
- this surge in LH is an example of a positive feedback because Estrogen stimulates LH leading to rapid increase in hormones that culminates in ovulation
- After ovulation, this + loop transitions back to negative as rising levels of progesterone inhibit effects on LH helping to regulate menstural cycle.
43
What is an example of a **negative feedback loop** in the **female cycle** ?
1. The hypothalamus is a gland in the brain that produces gonadotropin-releasing hormone (GnRH).
2. The GnRH signals the pituitary gland to produce follicle-stimulating hormone (FSH).
3. FSH triggers the ovaries to produce the hormone estrogen.
4. High levels of estrogen inhibit the production of GnRH. This causes the pituitary gland to make less FSH, which causes ovaries to make less estrogen.
5. This happens because it keeps their levels more or less constant.
44
Where do **behavioural differences** come from?
Sex differences in the brain
45
What is the **male** rat mating behaviour?
MOUNTING position
46
What is the **female** rat mating behaviour
LORDOSIS position
47
Tell me about **Davidson 1966**
| HINT : Rats
- Castration of male rats STOPS mounting behaviour
- testosterone replacement therapy restores mounting behaviour
- this suggests that mounting behaviour is controlled by circulating testosterone levels
48
Criticising **Davidson 1966**
- Injecting female rats with testosterone does **NOT INDUCE** mounting behaviour
- Injecting castrated male rats with estrogens and progestins does **NOT** lead to lordosis position
- Suggesting, there is more to mounting behaviour than circulating hormones.
49
What is an **Activational Hypothesis**?
The activational hypothesis suggests that hormones mainly trigger or modify existing behaviors** temporarily**, instead of permanently shaping how behaviors develop. In simpler terms, hormones activate or boost certain behaviors based on specific body or environmental signals.
50
What is an **Organisational Hypothesis** ?
The organisational hypothesis is an idea that suggests that early exposure to hormones during critical periods of development can **permanently** organize or "set" certain aspects of an individual's biology, including brain structure and function, as well as behavior.
51
Activational/Organisational Hypothesis :
Steroid hormones permanently organize the nervous system at some point during development. In adulthood, the same steroid hormones activate, modulate, or inhibit adult-typical male/female behaviors.
**Organisational effects** : During critical periods of development, steroid hormones permanently organise the structure and function of the nervous system.
**Activational effects** : In adulthood, these same steroid hormones can activate, modulate or inhibit behaviours that are already organised during development. This happens when hormones fluctuate e.g. menstrual cycle
52
Tell me about **Phoenix et al., 1959**
1. Preggo guinea pigs given testosterone, to affect the development of the offspring
2. In adulthood, the offpsring was gonadectomised (removal of gonads (testes or ovaries)), and then treated with either estrogen or testosterone to observe mating behaviour
3. Prenatally testosterone-treated females were LESS LIKELY to display the lordosis position
4. Prenatally testosterone-treated females were MORE LIKELY to display mounting behaviour when treated with testosterone as adults
THIS MEANS ...
**Organisational effects are permanent
Activational effects are acute and transient**
53
Are **Organisational effects** :
A : permanent
B : Acute and Transient?
**A : Permanent**
This means organisational effects have permanent effects on the structure and function of the nervous system - they occur at critical points of development.
54
Are **Activational effects** :
A : Permanent
B: Acute and Transient
**B : Acute and Transient**
Meaning they occur in response to fluctuations in hormone levels in adulthood and are temporary .
55
Tell me about **Grady et al., 1965**
1. Exposed rats to androgens prior to 10 days of age causes masculinisation and defeminisation of behaviour
2. If they ARE exposed to androgens their behaviour is demasculised and feminsied.
3. If administered after day 25, no amount of androgen can cause masculinisation (sexual maturity is reached at day 42)
4. **The are sensitive periods for organisational effects**
56
What does **Androgen exposure during adulthood** do?
Activates the previously programmed male behavioural patterns.
57
What does **Estrogen exposure during adulthood** do ?
Activates the previosuly programmed female behavioural patterns.
58
What does **Androgen exposure at critical points of development** do ?
Leads to defeminisation
59
What does **lack of Androgen exposure at critical points in development** lead to?
This leads to demasculisation
60
How is the **brain** defeminised or demasculinised ?
**Aromatisation **- the process where testosterone gets converted into estrogen in the brain.
61
What do **MASCULINE behaviours** depend on ? Give me 2 studies as examples
**Estrogen exposure**
1. **Grady et al., 1965** injecting rats with ANDROGENS into the blood stream prior to 10 days of age causes masculinisation of behaviour
2. **Booth, 1977** But an injection of ESTROGENS directly into the brain of rats before 10 days old masculinises later behaviour even more effectively than androgens.
62
Give me the study for **Aromatisation**
**Gorski, 1993**
Testosterone is aromarisied to estradiol in the brain, many behavioural effects are dependent on this conversion
63
Why are **females not masculinised**?
1. Estrogen production of fetuses/newborn rats is low
2. Rat fetuses produce ALPHA-FETOPROTEINS - this binds circulating estrogen and removes it via the placenta and maternal liver
3. Alpha-fetoprotein protects the fetus from estrogenic effects
4. Alpha-fetoprotein does NOT BIND to androgens, so testosterone from male fetuses reaches their brain where it is aromatisied to estrogen and then has masculinising effects.
64
What is **Alpha-fetoprotein**?
Produced by liver - protects the fetus from estrogenic effects
65
How does the** intra-uterine development** affect behavioural sex differences?
**Meisel & Ward, 1981** - uterine blood flow in rats from cervix to ovary, females who are 'downstream' in the uterus, meaning closer to the cervix and thus potentially receiving less blood flow or exposure to certain hormones from the placenta, were more susceptible to masculinising effects. This means that these female fetuses might exhibit more characteristics typically associated with males.
