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21 Cards in this Set

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Some sex differences in behaviour are due to sex hormones which lead to sex differences in the brain in early life. Early in development: masculinise/feminise brain and therefore influence behaviour

ORGANISATIONAL HYPOTHESIS - based on findings that exposing female rats an guinea pigs to androgen in utero during critical periods altered adult sexual behaviour.

OH - Young et al (1964) - early androgens organise developing CNS in a masculine way. Defeminisation/masculinisation.

Without effects of androgens, animals behave in female way - sex organs, brain and behaviour.

OH: NEURAL/BEHAVIOURAL SEXUAL DIMORPHISMS - Sexual dimorphisms in rodents have been demonstrated to depend on organising effects of androgens during critical developmental periods - these critical periods are shortly after birth

Other neural sexual dimorphisms have been demonstrated to depend on organising and activating effects on androgens and others only involve activating and reversible effects during adulthood.

Neural sexual dimorphisms contribute substantially to sex differences in behaviour (esp. reproductive) - often in conjunction with activating effects of sex hormones on sexual dimorphic neural systems.

Many instances of neural sexual dimorphisms described without obvious behavioural correlates and of behavioural sex differences (often produced by hormone effects) for which no neural substrates have yet been identified

Interaction between environment and hormonal influence on neural and behavioural sexual dimorphisms - NATURE AND NURTURE

Osterogen found to be as effective as testosterone in masculinising brain and behaviour in rodents. Many masculinisng effects of testosterone were mediated by oestrogen receptors

AROMATISATION HYPOTHESIS - testosterone - oestrogen. Based on these findings, suggested that the CNS cells testosterone is converted to oestrogen by an enzyme called aromatase before it acts on oestrogen receptors to exert masculinising effects.

PROTECTION HYPOTHESIS - explains why females don't masculinise even though they have oestrogen - brains of developing rodents are protected from indiscriminate masculinising action of oestrogen by an oetrogen binding protein, alpha-fetoprotein in the blood

Testosterone is not bound by the protein and can enter the CNS cells where it can be converted into estrogen and then exert its masculinising effects.

Bakkar et al (2006) - alpha-fetoprotein mutant mice show masculinised brains and behaviour

Male and female doesn't determine sexually sexually dimorphic behaviour - most behaviours show considerable overlap for M and F. Range of differences within each sex larger than that between

Largest behavioural sex differences are seen in sexual orientation and core sexual identity - these differences not absolute

Determinants of SD in B and C - genes, hormones, environment/experience (all differ between M and F) Interact in their effects on the brain to result in sex differences in behaviour.

SD in behaviour may be partly mediated by sexual dimorphisms in the brain or CNS

Or may result from exposure of identical brain substrates to female/male sex hormones and female/male experiences

Lordosis response: body posture adopted by some mammals, usually associated with female receptivity

Requirement for mating - attractivity, proceptivity (willingness) and receptivity (ability)

When all 3 factors present - COURTING BEHAVIOUR - SEX (consomatory behaviour)

Testosterone is necessary - castrated rodents don't show mating behaviour

Pregnancy is only possible during a certain time of the cycle (when oestrogen and progesterone levels high). Female sexual behaviour is linked with reproductive cycle and controlled by hormonal fluctuations (hormones released from pituitary gland, stimulate follicular development and lead to ovulation, ovum release, pregnancy.

Females can only mate during certain time of the cycle around ovulation except for primate females who can do so at any time. Even in primates, attractiveness, receptivity and procepitivity appear to be modulated by the hormonal cycle which may also influence behavioural, cognitive and affective functions that aren't directly related to reproductive behaviour.

SPINAL MECHANISMS - MALE COPULATORY BEHAVIOUR IN RATS - spinal nucleus of the bulbocavernosus (SNB) - collection of motor neurons in lower lumbar spinal cord - controls the bulbocavernosus muscle at base of penis (necessary for normal penile reflexes - Monaghan & Breedlove 1992)

They are absent/reduced in F compared to M

Nature & Nurture - Test exerts some masculinising effects on SNB and sexual behaviour via rat mother: blood test stimulates rat dam to lick male pups more often than female pups. Such anogenital licking contributed to normal male sexual behaviour in the adult and to a normal number of SNB neurones

BRAIN MECHANISMS - SEX CIRCUITS: contain sex hormone receptors = crtical for sexually dimorphic mating behaviour: testosterone for male behaviour, oestradiol and progesterone for female behaviour

Several components of these circuits are sexually dimorphic

Sexually dimorphic nucleus of the preoptic area (SDN-POA) and posterodorsalmedial amygdala (MePD). SDN-POA is masculinised by test during a critical perinatal period. MePD volume and cell size depend on testosterone action in adulthood.

Sex differences in human spinal cords - ventrolateral (VL) cell group of Onuf's nuclues in the human spinal cord. More motorneurones in males than females.

Fliers & Swaab (1985) - one nucleus in the POA of hypothalmus was larger in volume and cell number in males than females.

LeVav (1991) - no sig. sex differences in INAH1, 2 and 4. Replicated that INAH3 was larger in heterosexual men than in women. Found additionally that INAH3 didn't differ between homosexual men and heterosexual women.

Allen et al (1989) - studied four nuclei in the POA which they names interstitial nuclei of the anterior hypothalamus (INAH 1-4). INAH1 corresponded to SDN of F&S1985, but didn't differ between sexes. INAH4 also didn't differ. INAH2 and 3 were larger in men than in females.

SDs exist in CNS regions that have been implicated in sexually dimorphic mating behaviour - consistent with the idea that neural sexual dimorphisms may contribute to behavioural sexual dimorphisms

Organisational hypothesis - some aspects of SD mating behaviour and relevant neural SDs have been shown (in rodents) to involve organising effects of sex steroids during critical developmental periods

AGGRESSION - more in M than F. Threat/attack on other individuals? Aggression is not unitary but some aspects of aggression are strongly related to reproductive behaviour (e.g. competition, protection). These aspects mediated by brain regions which overlap with regions implicated in reproductive behaviour = SEX DEPENDENT and under influence of sex steroids (there is particularly strong evidence for a role of testosterone)

Effect sizes of differences in ratings of aggression and competitiveness based on questionnaire responses= physical aggression: asked on opinions of certain statement (physical statements), verbal (e.g. if someone annoys me) or interpersonal competitiveness (I dont feel like winning is important)

Test has been suggested to contribute to these sex diffs by acting on brain, and some direct evidence supports this suggestion (Pasterski et al 2007)

Male advantage in place learning and navigation (Astur et al 1998, Moffat el al 1998, Ionasson et al 2005) - evidence to support men have better spatial memory

Markowska (1999) - rats locate hidden platform from spatial cues; typically worsen with age; females always worse than males

Astur et al (1998 - human females make more errors and are less efficient. Males have an advantage in spatial navigation.

Prairie Voles - such differences may have evolved due to ecological pressures (only exist in polygamous species in which males range more widely than females in the field) and correlate with a larger hippocampus (spatial learning) in males - JACOBS ET AL 1990

Sex diffs in hippocampus have also been found in rats (Madeira & Lieberman 1995) and men (even though in rodents, the hippocampus tends to be larger in males than in females, whereas in humans the opposite is the case!)

Human fMRI study - men may use hippocampus more than women in order to navigate a (virtual) maze

Gladue & Bailey 1995 - mental rotation : 20 items with 2 correct and 2 incorrect choices each; 1 point per correct choice: max score 40.

Water jar task - 10 items consisting of a jar tilted at different angles, pps required to draw the water line assuming the jar is half full: max score 10.

Brain weight higher in males than females. If these SDs contibute to sex differences in behaviour and cognition it is unknown.

Affective disorders (except mania) and anxiety disorders are more prevalent in women. Substance abuse and antisocial PD are more prevalent in men (Table, Kessler et al 1994). ASD more prevalent in males than females.

Nature and Nurture exert reciprocal effects on each other (Halpern 2007)