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Chromosomes
Made of DNA and protein. Genetics. Female = XX
Male = XY
Testis determining factor
Gene SRY located on Y chromosome, turns fetal gonad into testis. In its absence, gonad becomes ovary
Anti-mullerian hormone
de-feminising hormone produced by early testis
Androgens
Masculating hormone produced by early testis
Summary of male sex determination
Testis determining factor turns primordial gonads into testis.
Mullarian goes due to anti mullerian hormones
Androgens cause wolfram system to develop, developing external genitalia develops
summary of female sex determination
Primordial develops into ovaries, no hormones needed. Mullarian system turns into internal genitalia. Wolfian system withers without androgens.
organisational hormones
Effect remains after hormone has been removed. Often occurs during sensitive period.
Eg wider pelvis in women, and wide shoulders/lower voice in men
Activation hormones
Effect is reversible, depending on presence or absence of hormone.
Eg increased facial hair/muscle mass in men, and increased breast development in women
Gondatopins
Release hormone of GnRH which starts off puberty. Which then signals FSH and LH
FSH
Male = sperm production
Female = follicles ripen
LH
Male LH = testosterone production
Female LH = induce ovulation
Hypothalami-pituitary-gonadal axis
Hypothalamus releases GnRH. GnRH signals pituitary gland to release FSH and LH. FSH and LH act on gonads stimulating production of sex hormones eg development of egg and sperm
Menstrual cycle
HPG axis. Follicles ripen due to FSH. Follicle produces estrodoil. This triggers FSH and LH to release ovulation. Ruptured follicle develops into corpus luteum, begins to release progesterone which prepares lining of uterus.
While ovum goes through fallopian tube due to rowing action of cilliated cells. If not fertilised, progesterone and estradoil levels fall and cycle begins
Androgen insensitivity syndrome
Gonads develop as testes. Androgen receptors don’t work so testosterone can’t do its normal job. Develop anatomically as a female, but without I real female genitalia. Puberty typically late. Typically identify as women
5a reductase defiency
Can’t convert testosterone into DHT, but at puberty the high levels of testosterone can mimic DHT. Develop male genitalia (guevedoces). After puberty, mostly identify as men
Congenital adrenal hyperplasia
High levels of prenatal testosterone in girls. Ambiguous external genitalia in girls. Some assigned male at birth. 5% of assigned females have gender dysphoria, whereas 12% of assigned male
Sex behavioural differences
toy preference, play style and prenatal testosterone.
Men faster in mental rotation tasks so is CAH. Suggesting role of testosterone
Sex structural differences
Male brains 10% larger. Female cortex thicker (more grey matter). Males larger white matter volume and subcortical structures (hypothalamus, amygdala etc)
Environmental effects on sexual orientation
Exposed in childhood, social effects (stereotypes). However little evidence this affects sexual orientation
Activation hormonal effects on sexuality
Testosterone levels, estradoil levels, menstrual cycle. However found it effects sexual motivation not orientation
Organisational hormones on sexuality
Prenatal hormones (testosterone). Cognitive performance = gay better at verbal but worse at spatial (male). Female gay better at mental rotation. Butch lesbians have more masculine 2D/4D.
Ota-acoustic emissions (when click, ears make sound back). Gay women closer to straight males.
CAH females more likely to be gay
Genetic effects on sexuality
Higher concordance in mz than dz twins
Gay men often have gay uncles in mother’s side suggesting X chromosome inheritance.
Evolutionary concerns = offspring
Fraternal birth order effect
The odds of having a gay son increases with the amount of sons you’ve had as a mother. So man is more likely to be gay if they gave more older brothers from the same mother
Maternal immune hypothesis
Mother’s immune response to protein neuroligin 4 Y-linked predicted probability of having gay son
Trans male genetic predisposition
Long version of estrogen receptor beta and adonosene version of estrogen receptor alpha
Genetic predisposition of trans female
Long version of androgen receptor and short version of estrogen receptor beta + alpha
Pre-transition brain differences
Brain volumes in line with natal sex.
MtF show more feminine cortical thickness.
FtM show more masculine basal ganglia and white matter tracts
Androstenedione
Can be converted into testosterone or estrogen for secondary sexual characteristics
gonad
Organ that produces gametes (reproductive cells) and hormones. Testes and ovaries
Preoptic area of hypothalamus
Regulates sexual behaviour and reproductive functions. Regulates GnRH
Kisspeptin
Peptide hormone that regulates puberty and reproductive function. Produced in hypothalamus
Vasapressin
Hormone produced in hypothalamus and released in pituitary gland, influences sexual behaviour
INAH3
Sexual brain region in hypothalamus, smaller in homosexual men
Anterior commissure
Fibres that connects two brain areas. Larger in women do better at verbal processing and emotional response
What determines a baby’s chromosomal sex
Presence or absence of Y chromosome
Persistent Müllerian duct syndrome
Individual has male external genitalia with testes.
Male and female internal genitalia
Consequences on the HPG axis of taking anabolic steroids
testes make low amounts of testosterone, the hypothalamus produces less GnRH, testes will shrink
Complete androgen insensitivity syndrome women
Leads to lack of pubic hair
what does anti-androgen drugs do to men?
Make a man uninterested in sex
What would you need to investigate to distinguish an activational from organisational effect of hormone treatment in transgender people?
Explain activation and organisation
Time of hormone treatment, if in adulthood more likely to be activational
Persistence after stopping hormones
Exposure history
Functional (activation) vs structural (organisational)
Longitudinal studies - tracks changes over time