Sex Differences in Behavioral Development

how are males and females different

body size, body type, mentally, and behaviorally; true for humans and non humans

what is also true for most sex differences

much overlap between the sexes; more variation within than between the sexes

sexual differentiation

becoming typically male or female

what is used to study early hormones involved in sexual differentiation

animal models

what does studying children cross culturally show about sex differences

indicate a biological basis

atypical sexual differentiation

occurs when chromosomal, gonadal, or anatomical sex development does not follow the typical path of a standard 46,XX (female) or 46,XY (male) pattern

why is studying atypical sex development difficult

hard to get enough cases, cases can differ in timing, cases can differ in severity, other medical conditions can confound

how might cases of sexual differentiation differing in timing make them hard to study

might emerge during conception, later in embryonic development, or later in fetal development; hard to determine if it happened earlier or later in brain development

chromosomal sex

we have two sex chromosomes

gonadal sex

if you have testes or ovaries/male or female typical gonads; may not be consistent with chromosomal sex

morphological sex

what does your body look like externally

behavioral sex

do you show more male-typical or female-typical behaviors

gender identity

what sex does one feel/think they are

gender role

what does culture dictate as your role, externally driven; where do you land

legal sex

how does the government see your sex; some states define it chromosomally, others based on gonadal or behavioral sex, others defined as identity; dependent on state and culture

who determines the baby’s sex

the father

when is chromosomal sex determined

at fertilization

germinal ridge

the early precursor to gonads, which develops into either testes or ovaries during embryonic development; the same between everyone early on in development

what determines what the germinal ridge turns into sex wise

a signal from a gene on the y chromosome that spontaneously turns on and signals it to become one gonad or another

what sex gets the signal to the germinal ridge

males

SRY gene

a gene located on the Y chromosome responsible for the development of male gonads and triggering androgen production, testis determining factor

what gene produces TDF protein

SRY

what happens if the germinal ridge is exposed to high levels of TDF

permanently turns into testes

what happens to the germinal ridge in the absence of y chromosome, therefore absence of SRY and TDF

can’t turn into testes, therefore turns into ovaries

how can we prevent male gonads from forming

can use a blocker for TDF (after the chromosomal level)

after gonads (testes/ovaries) are determined, what drives sexual differentiation

hormones

what causes body/brain/behavior to be driven in a male direction

fetal testes secreting androgens

what causes body/brain/behavior to be driven in a female direction

the absence of hormones being secreted by fetal ovaries

masculinization

the process by which male characteristics develop due to the influence of androgens from the testes, the development, biological process, or physical/social adoption of male-associated traits and characteristics

defeminization

potential female-specific structures, functions, or behaviors are altered or suppressed through male development processes, the reduction, removal, or reversal of feminine traits, physical characteristics, or roles

feminization

the process by which female characteristics develop due to the absence of androgens, leading to the development of female-associated traits and characteristics

demasculinization

the process by which male characteristics are reduced or suppressed, often through female development processes, leading to diminished masculine traits and behaviors

when do fetal ovaries begin to produce hormones

have very little capacity to until puberty

why is the female sex the default

in the absence of gonadal steroids, body/brain/behavior are feminized and demasculinized, germinal ridge turns into ovaries in the absence of the active mechanism

how does external genitalia undergo sexual differentiation

through hormones

genital tubercle

is a structure that develops into the clitoris in females and the fallus in males during sexual differentiation, begins as a bipotential, undifferentiated tissue

what happens to the genital tubercle if there are no androgens

clitoris and labia form

urogenital groove

could become either vagina or scrotum

if there are NO androgens present for the originally undifferentiated tissue, what happens

clitoris and labia form

if there ARE androgens present for the originally undifferentiated tissue, what happens

penis and scrotum form

dihydrotestosterone (DHT)

A potent androgen derived from testosterone, responsible for the development of male external genitalia and other male secondary sexual characteristics

what enzyme turns androgen into DHT

5-alpha-reductase

where is 5-alpha-reductase (5AR) found

in genital skin cells, even in females

how does 5AR work in male genital skin cells to masculinize them

in males that release testosterone from their fetal testes (makes a lot of androgen), testosterone goes into the blood and when it reaches the cells of the genital skin, the enzyme is made inside of the cells of the genital skin, and converts those testosterone cells into DHT and acts on the receptor to change the morphology of the tissue which reshapes itself to become a male penis and scrotum

what does genital skin always have regardless of sex

5AR

what makes female genitals easily masculinized

5AR that is in everyone’s genital skin

how are females easily masculinized

if there is testosterone in the blood regardless of sex, 5AR is going to convert it into DHT, and turn genitalia into a penis and scrotum regardless if you are female

Congenital Adrenal Hyperplasia (CAH)

excess androgens from adrenal glands rather than cortisol

what does CAH look like

clitoris is enlarged, vagina is not paved

adrenal gland

maks stress hormones such as glucocorticoid, cortisol, etc

before the 1990’s, what was the most common doctoral thought regarding girls with CAH/atypical sexual differentiation

genital surgery to correct external genitalia (cut off tip of clitoris → no sexual response), or remove ovaries of female, let external genitalia do their thing, then give them androgens during puberty so they can be raised as male

what does 21-hydroxylase enzyme in the adrenal cortex allow for

conversion of steroid hormone precursors (cholesterol) into cortisol

hypothalamic pituitary axis

The hypothalamic-pituitary-adrenal axis regulates stress response, linking the hypothalamus, pituitary gland, and adrenal glands in hormone production and release.

what happens when there is a mutation in the hydroxylase gene?

can’t make enzyme 21-hydroxylase

what happens when 21 hydroxylase can’t be made?

can’t get the conversion that leads to cortisol, but the steroid hormone precursors still have to make something, so they take a much less used steroid path and make androgens from the cholesterol instead

what normally happens in our bodies when cortisol is released

negative feedback loop to turn off the system after it goes into the blood

how does the negative feedback loop for cortisol work

hypothalamus has a lot of glucocorticoid receptors, and when they detect the cortisol and think there’s enough, the whole system shuts down until it’s activated again when cortisol levels get low

in people with CAH, how does the negative feedback loop for cortisol work

Due to the lack of cortisol production, the hypothalamus does not receive the signal that cortisol levels are sufficient, leading to continuous stimulation of the adrenal glands and excessive production of androgens being put into the blood, disrupting the feedback regulation

how does the disrupted negative feedback loop in people with CAH lead to external genitalia and the brain being masculinized

androgen levels become so high because the hypothalamus drives the anterior pituitary even more because the system is looking for cortisol but can’t find it, so androgen is put out in even higher amounts

complete androgen insensitivity syndrome (CAIS)

genetic males with androgen receptor gene mutation, there is lots of testosterone, but not way to detect it; they look like girls externally, but still have testes in their abdomen, completely look female and have female brains

why does external genitalia in people with CAIS look completely female

no androgen receptors, DHT couldn’t bind to androgen receptors which would need to happen

how are most cases of CAIS reacted to

raised as girls, remove testes and administer estrogen and progesterone to help turn the rest of her body female

5-alpha-reductase deficiency

genetic males without the enzyme to convert T into DHT; external genitalia can’t be masculinized

in those with 5AR deficiency, what sex are they raised as

female

what happens at puberty for those with 5AR deficiency

testes secrete testosterone levels so high that it overrides the need for conversion to DHT and masculinizes genitals

what society has no problem with 5AR deficiency

dominican republic, there was a mutation that was passed down to a significant level of the population

what are people with 5AR deficiency in the Dominican Republic called

guevedoces

how does the brain become typically male or female

with fetal testosterone, it’s masculinized, without fetal testosterone, it’s feminized

during early development, what sex is the brain

undifferentiated

what is the organizational/activational hypothesis to explain origins of sex differences in brain/behavior

differential exposure to hormones during early development alters neural machinery for behavior, differential exposure to hormones during adulthood then activates that “machinery”, leading to behavior

what does activation mean in terms or organizational/activational hypothesis

the process by which hormones influence and trigger specific behaviors in an individual after the initial organization of neural circuits during development, refers to the part of adulthood where sometimes you don’t see differences until after puberty

how do female brains react to the organizational/activational hypothesis

female brains are female-organized, and the brain is then activated by ovarian hormones during puberty and throughout adulthood that can allow the expression of the female brain

what is an example of activational/organizational hypothesis in female rats

injecting them with a lot of testosterone on the day of birth, then injecting them again during puberty to activated the organized brain from earlier on, they show male-like behavior such as mounting

what happens activationally if female rats were injected with placebos the day of birth instead of testosterone, but then injected with testosterone during puberty

not nearly as dramatic of a difference; need a male organized brain to behave like a male after puberty

what happens to ovaries when females are injected with testosterone upon birth

sterile, ovaries don’t function because the brain mechanism that controls ovulation doesn’t function properly

what happens to male rats when they are castrated upon birth (O/A)

removes the source of testosterone that would organize/masculinize their brain to be male

what happens to castrated male rats when injected with estrogen in adulthood (O/A)

brain is activated in a female like way, prevented their brains from being masculinized, resulting in feminine behaviors and physiological responses such as lordosis

what happens to male rats who were organized male (not castrated at birth) when injected with estrogen later in life?

doesn’t do anything, don’t show female behavior

what is necessary for the pubertal activation (O/A)

removal of testes/injection of testosterone to organize the brain

what was the first reported physical sex difference in the brain

medial preoptic area (mPOA)

what physical sex difference is shown via the mPOA

females have more synapses on dendritic spines, fewer on dendritic shafts than males, females have more synapses on particular sites than males and vice versa, physical size difference

where is the mPOA located

subnuclei of hypothalamus

how is the size of the SDN POA different in sexes

5 - 7x larger in males than females

how can the SDN POA masculinize females

with neonantal testosterone, doesn’t become quite as large as in males, but close

what happens to the SDN POA if you castrate the male on day of birth

it’s smaller, not as small as it would be in a typical female, but effective

when is the critical period for reorganization

first day postnatal or before born

what effect is the size of the SDN POA purely reliant on

organizational, doesn’t require activation to maintain a certain size

SDN POA

sexually dimorphic nucleus of the POA

how do the number of cells in the preoptic area differ before the period of sexual differentiation

they have the same number, they don’t

how can BrdU be used to see sexual differentiation

look at how many cells were born on days during prenatal development

when is there a natural surge in rats and mice of testosterone

embryonic days 17/18, a few days before birth

what happens in response to a massive natural surge of testosterone in rats a few days before birth

males have a massive amount of neurogenesis/cell birth in the preoptic area, leading to a larger SDN POA

why is the SDN POA smaller in females than males

don’t have a massive surge of cell division/cell birth/neurogenesis because don’t have testosterone which causes it, cells dying because of the absence of early testosterone

what happens to cells in the absence of early testosterone

cells become feminized

what happens to cell death in early development for males in the mPOA

testosterone is neuroprotective, fewer cells die

what are some more examples of differences in vertebrate brains that could all contribute to sex differences in basal and stimulated brain activity

neurochemicals, expression of neurochemical receptors, anatomical connectivity between brain cells/sites

how does connectivity differ between sexes

input to mPOA differs, and number of axons between site A and site B differ between sexes; stronger projection from A to B in males than females

INAH

Interstitial nuclei of anterior hypothalamus (in the POA)

what are the size differences of INAH between sexes

INAH-3 (and possibly 2) is 2-3x larger in men

how is the INAH affected by sexual orientation

INAH 3 of gay men was smaller than straight men, but not as small as female version