Reproductive behaviour Flashcards
reproductive behav
Sexual selection
- Preferential reproduction in some indv which changes traits that get represented in popn - leads to:
Sexual dimorphism
- Diff between males and females
All organisms evolved to reproduce
early development
Primary sexual characteristics – i.e. internal and external genitalia.
Sry gene causes male internal genitalia - testes.
No Sry gene causes female internal genitalia - ovaries.
Hormones from testes have an organisational effect promoting masculinisation and defeminisaton.
Initially foetuses identical other than genes
Sry gene within Y chromosome
Females = absence of hormones – default
Males are slightly modified female
see notes
hypothalamus - arcuate nucleus
Puberty is initiated by the arcuate nucleus of the hypothalamus – time-keeper for initiation of puberty
kisspeptin causes the anterior hypothalamus to release Gonadotropin-releasing hormone (GnRH).
see notes
pituitary - GnRH
GnRH causes pituitary to release FSH and LH in both sexes.
FSH and LH cause testes to release testosterone and ovaries to release estradiol.
These hormones drives the development of sexual maturation.
see notes
hypothalamus and pituitary - master endocrine system
Hypothalamus and pituitary are the master controllers of the endocrine system.
Communicate via hormones in the blood releases into circle of Willis.
Play an organisational and activational role.
Optimal position to release hormones into bloodstream
see notes
hormonal control of sexual behav
Hormonal control of the menstrual cycle.
The combination of estradiol + progesterone and signals the fertile phase of the female’s cycle.
The combination of E+P promotes sexual behaviour in females
Fertile = produce progesterone and estradiol – promotes sexual behaviour
rat sexual behav
Rats show species specific sexual behaviour sequences (humans are a bit more variable).
- Proceptivity – female approach
- Attractiveness – male engagement/mounting
- Receptivity – female willingness
- Lordos – female posture
hormonal control of sexual behav
The Interaction between activational and organization effects is revealed by a series of experiments.
Males and Females are gonadectomised at birth and either given hormones at that time (to study organisational effect) or in adulthood (to study activational effects) – brain cannot develop in same way
Table shows that gonadectomised males need replacement hormones at birth in order to show activational effects in adulthood.
see notes
Organisational = need hormone when developing in order to have substrate that makes you sensitive to activational effect of hormones when post-puberty – actually have effect on behav
Need testosterone at birth to have organisational effect
Testosterone defeminises brain
human sexual behav
Females are more attractive when they are in the fertile (luteal) phase (progesterone+estradiol).
Raters of both sexes rated the attractiveness of female pictures taken during the follicular and luteal (fertile phase).
Circa 5% preference for fertile females
see notes
Is the data robust?
Initiation of sexual activity between human partners.
Males initiate sex evenly across the female menstrual cycle.
Females initiate sex more often during ovulation (the fertile phase)
see notes
Previous research doesn’t converge into more initiation by males in the fertile phase
What do females prefer in men when they are fertile vs. non-fertile?
Rate qualities as a one-off sexual partner
They show a greater discrimination in their preference for signals of male dominance and genetic quality/compatibility.
MHC = Major histocompatibility complex – mis-match between immune systems between 2 genders
see slides
male sexual behav - Bagatell et al. (1994)
Male administration of a GnRH antagonist (Nal-Glu) blocks testosterone production and sexual behaviour in males, but not if given replacement T
see slides
Reduced freq of sexual desire, intercourse, fantasies and masturbation with antagonist alone – losing testosterone
sexual orientation
Male heterosexual = brain masculinized and defeminized
Female heterosexual = neither masculinized nor defeminized – left alone – default
Male homosexual = neither masculinized nor defeminized
Female homosexual = brain masculinized and defeminized
Male and female bisexual = masculinized but not defeminized.
physical morphology
congenital adrenal hyperplasia (CAH)
androgen insensitivity syndrome
heritability
physical morphology - Balthazart (2016)
Individuals who prefer woman (heterosexual males and lesbians) have been masculinised and defeminised, and have a masculine index to ring finger ratio (and longer limbs).
Individuals who prefer males (heterosexual woman and homosexual men) have been feminized and have a feminine index to ring finger ratio (and short limbs).
CAH
Abnormal androgens in genetic females.
Produces ambiguous genitalia.
≈33.3% genetic females with CAH identify as homosexual or bisexual compared to ≈2% of females as a whole.
androgen insensitivity syndrome
Testosterone should masculinisation and defeminise morphology.
Genetic males with androgen insensitivity syndrome develop as females.
They may be complete or partial females depending on the level of insensitivity.
Typically female external genitalia, but also with testes (internal) and without uterus or Fallopian tubes.
Typically favour male partners as do heterosexual females, suggesting neural feminisation.
heritability
Estimates of concordance rates for homosexuality in male and female identical twins and fraternal twins.
Suggest that there is a genetic influence on homosexuality.
However, if homosexuality was was perfectly heritable, the concordance rates for identical twins should be 100%.
50% role for psychosocial learning – less well understood
see notes
