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270 part 3 > sexual behaviour > Flashcards

sexual behaviour Flashcards

1
Q

SRY gene

A

on male Y chromosome – causes gonads to develop into testes

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2
Q

androgens (early, by testes)

A
  • increase testes growth (positive feedback during early development)
  • wolffian ducts develop into seminal vesicles & vas deferens
    =penis & scrotum development
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3
Q

Mullerian ducts

A

precursor to F structures: oviducts, uterus, upper vagina

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4
Q

testes, ovaries, adrenal glands produce

A

Testes: produce androgens > estrogens
Ovaries: produce estrogens (most prominent: estradiol) > androgens
Adrenal glands: both

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5
Q

effects exerted by steroid hormones

A
  1. Bind to membrane receptors i.e. NTs  rapid
  2. Enter cells & activate certain proteins in cytoplasm
  3. Bind to receptors that bind to chromosomes  activate/inactivate certain genes
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6
Q

Progesterone

A

prepares uterus for implantation of a fertilized ovum & promotes maintenance of pregnancy

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7
Q

Organizing effects of sex hormones

A

long lasting structural changes

Short term exposure: no apparent effect
Long term: limited changes in behaviour

–set the stage for activating effects (i.e F hypothalamus – later hormones can activate menstruation cycle)

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8
Q

Sensitive period for organizing effects of sex Hormones

A
  • first trimester – sex H determine M/F genitals & alter brain development
  • Puberty: F—breast size; M – facila hair, penis growth; changes in voice + some brain anatomy differences increase – persist despite conc of sex H declines
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9
Q

Activating effects

A

more temporary, continuing only when a H is present / shortly beyond
- i.e. H level influence degree of sex drive
- pregnancy: temporary effects on emotional arousal, aggressive behaviour
- mood changes over menstruation cycle
T / E2 levels modify behavior temporarily – behaviour influences hormonal secretions i.e oxytocin released by sexual pleasure

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10
Q

differentiation of external gonads depend mainly on

A

on testosterone

  • high = M (certain enzymes convert T to dihydrotestosterone – more effective at promoting penis growth  high dihydroT = tubercle grows into penis + scrotum )
  • low = F (low dihydroT = clitoris+ labia)
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11
Q

masculinzation of female rats (T injection)

A

T begins masculinizing the external genitals during the last several days of pregnancy & first few days after birth – rate declines after)
• F rat: partly masculinized if injected with T (larger clitoris, mounts sexually receptive Fs & make copulatory thrusting movements; T inhibited arching of back & allow being mounted)

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12
Q

inject male rats with E2 before birth

A

M rat: little effect if injected with Estrogens; but if lack androgen receptors (castration, genetic etc) – F anatomy & behavior

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13
Q

estradiol & some genes highly activated in F strongly affect

A 
uterus development (not external genitals)  
•	Genetic F that lacks E2 during early life: normal external anatomy (E2 not important for external anatomy), abnormal sexual behaviour / internal anatomy
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14
Q

sex differences in brain

A
  • Parts of F hypothalamus generate a cyclic pattern of H release (menstruation) – M: hypothalamus release Hs more steadily
  • Sex Hs act in different ways for different areas
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15
Q

alpha-fetoprotein

A
  • Early development in rats: high levels of alpha-fetoprotein in blood  bonds to circulating E2 & prevents it from entering cells
    • Female brain is not exposed to E2 at this time
    • Male : T is free to enter the hypothalamus – aromatase converts much to E2 (E2 exerts masculinizing effects at this time )
    –> sex differences in brain (mPOA, VMH, AN, anterventral PVN)
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16
Q

Medial preoptic area difference

A
  • Both T and E2 increase production of prostaglandin E2

- increases microglia, dendritic spines, synapses in males

17
Q

Ventromedial hypothalamus

A

contributes to aggressive & sexual behaviour & inhibits feeding (decreases insulin)
- E2 activates an enzyme (PI3 kinase) – increases release of GLUT from presynaptic neurons = increased branching in postsyn neurons in males

18
Q

Arcuate nucleus & anteroventral periventricular nucleus

A

more dendritic spines & synapses in Females (important for F sex behaviour)
– low E2 levels in early life : - E2 increases GABA production – acts on astrocytes to decrease dendritic spines

19
Q

humans: T acts on?

A

T acts on hypothalamus directly (instead of by conversion to E2

20
Q

activating effects – Sex hormones bind to receptors – effect?

A

increase responses in parts of hypothalamus (VMH, medial preoptic area (MPOA), anterior hypothalamus)

  • T primes MPOA & others to release dopamine (during sexual arousal: more dopamine = more likely to copulate)
  • Level of T corr positively with men’s sexual arousal & drive to seek partners
  • Both M & F: higher T levels = more likely than average to seek additional sex partners
21
Q

sexual desire in women

A
  • Menopause (decrease in E2 levels)/ surgical removal of ovaries : decrease in sexual desire
  • Restoring E2 levels: increases sexual desire
  • Administer T to levels far above normal: increases sexual desire
     but sexual desire correlates strongly with E2 not T
  • Periovulatory period (middle of menstruation cycle): E2 levels peak sharply
22
Q

pregnancy hormones: oxytocin & prolactin

A
  • Delivering baby: increase secretion of oxytocin & prolactin
     promotes milk production & maternal behaviour
     prolactin inhibits leptin sensitivity (eats more)
  • Pattern of hormone receptors changes
    • Late pregnancy: E2 sensitivity increases in MPOA, anterior hypothalamus, nucleus accumbens (areas important for maternal behaviour)
23
Q

after pregnancy: Vasopressin

A

Vasopressin (syn by hypothalamus, secreted by posterior pituitary)
 promotes social behaviour (i.e. male prairie voles: high vaso, long term bonds with female + help rear young)

24
Q

congenital adrenal hyperplasia

A

over development of adrenal glands from birth
intermediate appearance due to atypical hormone pattern
– genetically unable to produce cortisol : pit continues to secrete more ACTH  adrenal secretes more Hs inc T
genetic F exposed to more T – partly masculinized

25
Q

individuals with XY chromosome but lack androgen receptors (androgen insensitivity / testicular feminization )

A

have testes internally – no menstruation (but has other puberty changes)
if assigned as girls – many demand reassignment as males

26
Q

5a-reductase 2: enzyme that converts testosterone to dihydrotestosterone – effects if absent?

A

enzyme that converts testosterone to dihydrotestosterone  more effective than T for masculinizing the external genitals
Case: genetic male cannot produce the enzyme
- appear female at birth
- brain exposed to male T levels during early development
- puberty: T levels increase sharply  growth of penis & scrotum

27
Q

Sexual orientation

A
  • people discover their sexual orientation

• most men discover early; many women are slower

28
Q

homosexuality in twin studies

A
  • Homosexuality has a stronger concordance (agreement) for monozygotic than dizygotic twins
     mono twins are more likely to have the same sexual orientation
29
Q

Possible: sex orien depends on T levels during a sensitive period of brain development – hypotheses?

A
  • Mother’s immune system may exert prenatal effects
    • Probability of a homo orientation is slightly higher in men with more older biological brother
    • Hypothesis: mother’s immune system reacts against a protein in a son & attacks subsequent sons enough to alter development
  • Stress during pregnancy
    • Animals: prenatal stress alters sexual development
     daughters were normal
     sons had male anatomy but arched back to another M in adulthood
30
Q

sexual orientation & hormonal levels

A

NOT correlated:

similar hormonal levels in heteroM /F and homo M/F

31
Q

stress effects on T

A
  • releases endorphins: antagonize effects of T on hypothalamus
  • elevates levels of certain adrenal Hs (rats: corticosterone; humans: cortisol)
    • decrease T release
32
Q

differences in brain anatomy b/w homo & heterosexual men

A

relative to hetero, homo men tend to have:

  • larger anterior commissure (in F too)
  • larger SCN
  • smaller third interstitial nucleus of anterior hypothalamus (INAH 3) (has • possible role in M sex behaviour )
33
Q

oxytocin

A
  • stim contractions of uterus during childbirth, milk production, maternal behaviour, social approach, pair bonding
  • “love (enhancing) hormone” – both M & F release it during sexual activity
  • in men: enhanced attraction & fidelity to partner
  • helps with facial recognition & emotion expression recognition
  • increases conformity to “in-group” opinions
    but not always pro-social
  • increases attention to possible dangers &negative reactions when perceived as being threatened
34
Q

frontotemporal dementia

A

part of frontal & temporal lobes of cortex gradually degenerate
• damage often includes ventromedial prefrontal cortex& orbitofrontal cortex
 evaluation of reward & others’ emotional expressions – impaired
 show little empathy / concern

35
Q

monogamy in male prairie voles

A

non-monogamous males: higher expression of AVP (hormone released by post pit) receptor in lateral septum – increase expression: shifts to monogamy direction; monogamous males: higher expression in ventral palladum

36
Q

Japanese quail study

A

in castrated male quails, a T implant would gradually (genomic effects) restore time spent at window looking at a female (a appetitive sexual behaviour measure), injecting VOR (aromatase inhibitor) will cause the time at window to gradually decrease
– E2 (converted from T by aromatase) has genomic effects
E2 also has non genomic effects:
single injection of VOR vs VOR+E2: VOR decreases time at window after 30 min, but that decrease is not observed in group with E2 also injected

270 part 3 (3 decks)

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