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PSYC 304 - SEM 2 > Sex > Flashcards

Sex Flashcards

1
Q

what are steroid hormones?

A
  • means of communication in the body for organs that are not directly connected
  • hormones are released by glands into the bloodstream, and then they go to organs with appropriate receptors
  • they are derived from cholesterol and lipid soluble, meaning they can go inside the cell
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2
Q

how do steroid hormones work?

A
  1. steroid goes inside the cell and binds to receptor
  2. steroid receptor complex goes inside nucleus and binds to DNA
  3. increase gene transcription (protein synthesis)
    - they work on a slow time frame, slower than peptide/amine hormones, but have a longer lasting effect
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3
Q

what are steroid receptor co=factors?

A
  • can alter the type of protein the steroid signals the cells to make
  • the same hormone can promote synthesis of different proteins in different cells depending on the co-factors
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4
Q

what are the gonadal sex hormones?

A
  1. androgens
  2. estrogens
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5
Q

what are the characteristics of androgens?

A
  • testosterone is the most common
  • dihydrotestosterone is a much more potent form of T
  • testes release much more androgens than estrogens
  • also released in small amounts by the adrenal cortex
  • adrenal corticosteroid secretion inhibits androgen release (part of negative feedback loop)
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6
Q

what are the characteristics of estrogens?

A
  • estradiol is the most common
  • ovaries release much more estrogens than androgens
  • also released in small amounts by the adrenal cortex
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7
Q

what is the process in which gonadal hormones are released?

A
  1. hypothalamus
  2. GnRH
  3. anterior pituitary
  4. LH, FSH
  5. gonads
  6. sex hormones
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8
Q

what are the chromosomal make up of females vs. males?

A

FEMALE = XX
MALE = XY

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9
Q

how does the Y chromosome cause a fetus to develop as male? when does this happen?

A
  • Y chromosome has SRY gene and codes for SRY protein
  • this shows up at week 7 of development and causes testes formation
  • no SRY = ovary formation
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10
Q

which ducts are involved in male/female fetal development?

A

FEMALE - mullerian duct
MALE - wolffian duct

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11
Q

how exactly are the testes developed?

A
  • the SRY protein causes the medulla (inside) of the gonads to grow into testes
  • lack of SRY protein causes cortex of gonad to grow into ovaries
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12
Q

how does the XX chromosome cause a fetus to develop as female?

A
  • no Y chromosome = no testosterone
  • no testosterone = wolffian ducts shrink, mullerian ducts grow
  • the mullerian ducts form fallopian tubes, uterus, part of vagina
  • starts around week 7
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13
Q

once the testes form, how does this affect development?

A

testes form and make testosterone and anti-mullerian hormone (AMH)
- AMH causes Mullerian ducts to shrink while testosterone causes Wollfian ducts to grow
- occurs around week 7
- T masculinizes prostate gland, scrotum, and penis
- 5a-reductase converts testosterone into DHT
- dihydrotestosterone (DHT) stimulates testosterone receptors and is very strong

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14
Q

so what determines sex?

A
  • development into phenotypic male or female is controlled by presence or absence of testosterone
  • sex chromosome controls sex of the gonad
  • gonadal hormones determine sex of the rest of the body
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15
Q

what is androgen insensitivity syndrome?

A

occurs in people with XY chromosomes
- genetic defect with no functional androgen receptors so no effect of T in development
- testes form because of SRY from Y chromosome, but remain internalized
- mullerian ducts atrophy because of AMH from tests, but wolffian ducts do not develop (because no testosterone)
- female external genitals develop
- secondary sex characteristics develop from estrogen from adrenal glands and tests
- look and behave like XX genetic women on outside but no menstruation and no body hair

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16
Q

what is androgenital syndrome?

A

occurs in people with XX chromosomes
- caused by congenital adrenal hyperplasia
- individuals don’t produce cortisol, which inhibits T, meaning there is higher T than normal
- T masculinizes the fetus
- ovaries are still formed because lack of SRY protein
- wolffian and mullerian ducts grow
- external genitalia are intersex
- gender identity depends on amount and timing of T release

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17
Q

what are the steps of sexual behaviour in rats?

A
  • women control sexual encounters, and ovulate every 4-5 days
    1. during ovulation, female displays prospective behaviours (darting, hopping, ear wigging)
    2. male begins to mount receptive female
    3. female arches her back, moves tail to one side (lordosis)
    4. male then intromits (inserts penis) and thrusts
    5. repeat steps 2-4 until male ejaculates
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18
Q

what are female and male rats’ stereotyped sexual behaviours? what do these behaviours tell us?

A

FEMALE = lordosis, darting, hopping, ear wigging
MALE - mounting, intromissions
- primary measures used to index whether the sexual brain has developed more male-like or female-like

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19
Q

what are the two ways that sex hormones regulate sexual behaviour?

A
  1. organizational effects - changes in body/brain occurring during development
  2. activational effects - changes in body/brain after development
20
Q

what are organizational effects?

A

changes in the body/brain during development
- changes are permanent
- hormones exert effects during critical period of development
- in utero and in puberty for humans

21
Q

what are activational effects?

A

changes in the body/brain after development, usually after sexual maturity (puberty)
- transient effects that vary with amount of hormones in bloodstream
- brain areas are turned on or off by hormones

22
Q

when does development for part of the rat brain responsible for male/female sexual behaviour occur?

A
  • occurs 7 days after birth, unlike humans and primates
  • like development of the body, sexual brain development is regulated by presence or absence of testosterone
  • no androgens during critical period = female neural development by default
23
Q

how can male rats sexual behaviours be altered?

A
  • remove testes in the first week after birth (organizational effects)
  • de-masculinizes and feminized behaviour in adulthood
  • males don’t show stereotyped behaviours
  • replacement T in adulthood does not reinstate male-like behaviours
  • giving estrogens to adult male rats can induce female behaviours (activational effects)
  • not observed if rats are castrated after puberty
24
Q

how can female rats sexual behaviours be altered?

A
  • give T to female rate in the first week after birth
  • de-feminizes and masculinizes sexual behaviour in adulthood
  • females don’t show stereotyped behaviour
  • giving T in adulthood induces male behaviour
  • effects are not observed if T is given after puberty
  • giving estrogen to a neonatal female can also cause male patterns of behaviour, why?
25
Q

what is the aromatization hypothesis?

A
  • male rat fetuses release T from testes
  • T gets into brain and is converted to estradiol in the brain by the enzyme aromatase
  • early exposure to estradiol (not T) masculinizes rat brain
26
Q

why doesn’t mother’s estrogens masculinize female fetuses?

A
  • a-Fetoprotein is in the blood of male and female neonates
  • binds to free floating estradiol, prevents entry into brain
  • does not bind to androgens, T is allows to enter brain and be converted to estradiol
27
Q

what are some pieces of evidence for the aromatization hypothesis?

A
  1. neonatal estradiol masculinizes behaviour - saturates a-fetoprotein molecules and extra estradiol can pass into brain
  2. enzyme aromatase is present in neonates
  3. blocking aromatase or estrogen receptors disrupts masculinizing effects of T
  4. female a-fetoprotein knockout mice show more male/less female like behaviour
  5. dihydrotestosterone (DHT) cannot be converted to estradiol, has no masculinizing effects when given early in development in rats
28
Q

how does a-fetoprotein work in primates and humans?

A
  • a-fetoprotein is not responsible for protecting the primate/human from estrogens
  • development of primate sexual brain occurs in utero
  • in humans/primates, a-fetoprotein does not bind to estrogen
29
Q

what is the sex hormone binding globulin (SHBG)?

A
  • protects fetal primate brains from estrogens by binding to them
  • early treatment with either estrogens or androgens in pregnant primates can masculinize behaviour of female offspring (unlike rats)
  • synthetic estrogens that are not blocked by SHBG can also masculinize the primate brain
30
Q

what brain area is largely responsible for sexual behaviour?

A

preoptic area (POA) of hypothalamus
- large lesions of entire area disrupts sexual behaviour in males and females
- the sexually dimorphic nucleus (SDN) of the POA is larger in males than females

31
Q

how do the amount of hormones effect the size of the sexually dimorphic nucleus (SDN)? does lesioning the SDN-POA affect sexual behaviour?

A

T injections in females = bigger nucleus
castration in males = smaller nucleus
- selective lesions of SDN-POA do not have major impact on sexual behaviour
- SDN is most important in development and less in behaviour
- changes in SDN may go on to change other brain areas

32
Q

how does sexual orientation develop?

A
  • sexual orientation is determined early in development and due to biological factors
  • prevalence ranges from 2-10%
33
Q

what do twin studies tell us about the heredity of homosexuality?

A
  • males = 52% of monozygotic, 22% of dizygotic twins are both homosexual
  • females = 46% monozygotic, 16% of dizygotic are homosexual
  • shows us that genes aren’t the only factors in play
  • they may be a gene near the end of the X-chromosome (Xq28) that influences male sexual orientation
34
Q

do our hormone levels vary with sexual orientation?

A
  • homosexuals and heterosexuals do not differ in hormone levels
  • but, in animals neonatal castration or perinatal T can cause same sex preference
35
Q

what is some evidence that hormones can lead to changes in sexual orientation in humans?

A
  • lesbians tend to show markers indicative of fetal androgen exposure
  • early exposure to synthetic estrogens may lead to women being more amenable to same-sex encounters
  • for gay men, there is a lack of evidence for fetal androgen exposure being responsible for orientation
36
Q

what are some indicators of homosexuality that are not correlated with early hormones?

A
  • gay men are more likely to be left-handed
  • with every successive son, chances of being gay increases by 22%
37
Q

what are some brain differences between heterosexual and homosexual men?

A
  • region of the anterior hypothalamus is larger in heterosexual men than homosexuals
  • but there were problems with the sample because many participants were AIDS victims
  • there may be more anatomical differences in brain structures for both gay men and women
  • there are differences in brain connectivity between homosexual vs. transgender individuals
38
Q

how do the activational effects of hormones affect male sex behaviours?

A
  • removing testosterone eventually reduces sex drive
  • replacement T brings sex drive back to normal
  • relative sex drive and T levels are uncorrelated in normal males, and T injections do not increase sex drive
  • could be because they already have a lot of T (more than 10x what they need)
39
Q

what is the Guinea pig experiment testing activational effects of hormones in men?

A
  • rated sexual activity of males as low, medium, and high
  • castrated all males then monitored sexual activity
  • all males then receive same large dose of T injections
  • large test dose restored all males to previous level of sex drive
  • other factors control individual differences in sex drive
  • some T is necessary, but more T does not mean more sex drive
40
Q

how does the male rat brain get ready for sexual behaviour?

A
  • sufficient levels of T in bloodstream primes brain regions to make them receptive to sexual stimuli
  • in males, T is converted to an estrogen which stimulates the mPOA, medial amygdala
  • when estrogen primes these cites, they can respond to sexual stimuli
  • olfactory signal -> medial amygdala -> mPOA -> ventral midbrain -> motor centres -> spinal cord
41
Q

what is some evidence that testosterone and estradiol regulate male rat sexual behaviour?

A
  1. mPOA/medial amygdala lesions disrupt sexual behaviour
  2. mPOA stimulation initiates sexual behaviour
  3. in castrated males, administration of T or estradiol into the MPOA reinstates sexual behaviour
    - androgens get brain areas ready to act in response to sexual stimuli, they do not cause behaviour but they are necessary for it
42
Q

how do hormones change in the female rat to reach ovulation?

A

in female rats,
- estradiol increases 2 days before ovulation, causing brain to make progesterone receptors
- progesterone then starts to increase, which plays an activational role
- when both peal, ovulation occurs and female shows stereotyped behaviours

43
Q

how does the female rat brain regulate sexual behaviour?

A
  • ventromedial hypothalamus (VMH) monitors changes in hormonal levels
  • estradiol causes VMH neurons to alter dendrites and make progesterone receptors
  • stimulation of progesterone receptors causes VMH cells to produce proteins necessary for lordosis
  • changes in VMH makes downstream nuclei more excitable
  • eventually signals output through spinal cord and promote lordosis in response to stimulation from mounting
44
Q

what is some evidence that estradiol regulates female rat sexual behaviour?

A
  1. VMH/PAG lesions disrupt lordosis
  2. implantation of estrogens into VMH reinstates lordosis in females with no ovaries
    - this pathway is for particular motor program, other sexual behaviours are mediated by other brain circuits
45
Q

how do estrogens affect human female sex behaviour?

A
  • human female sexual behaviour may or may not be tightly linked to estrogens
  • ovariectomy does not have reliable effects on sexual motivation and beahviour
  • suggests that sexual behaviour may be driven by hormones and not ovaries
46
Q

how do androgens affect human female sex behaviour?

A
  • testosterone levels can correlate with measures of sexual motivation
  • following ovariectomy, replacement injections of testosterone rekindles sexual motivation
  • androgens may be more responsible for sexual motivation than estrogens
47
Q

how does female sexual behaviour change during their menstrual cycle?

A
  • greater probability of having intercourse and achieving orgasm as ovulation approaches
  • not necessarily due to estrogen/progesterone, just dependent on menstruation
  • testosterone also increases during ovulation
  • when not ovulating, women preferred the scent of their partner but when ovulation, women preferred the scent of a stranger

PSYC 304 - SEM 2 (2 decks)

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