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Psych

TermDefinition
Gender Identity how you feel/present
Genetic Sex male: xy female: xx
Sex assignment what you're assigned at birth
Sexual orientation romantically attracted to
Chi-square ((o-e)^2)/e  the sum of all squares compares observed vs expected frequencies
DHT-dihydrotestosterone helps develop penis and scrotum
Testosterone helps develop van deferens , epididymis and vesicles
Degrees of freedom (row-1)(columns-1)
Mullerian duct uterus, fallopian tube + vaginal burrow, clit, vaginal lips
Wolffian duct vas deferens, epididymis, + penis and scrotum
Female hormones estrogen + adrenal androgens
Male hormones androgens (testosterone and others)
SRY sex determining region of the Y chromosome (causes testes and production of androgen, Mullerian inhibiting substance MIS)
Turner Syndrome single X chromosome, short, chest is shield like, nipples far, webbing around the neck (sex assignment is female and no ovaries)
Androgen insensitivity syndrome missing receptor (doesn’t respond), have testes but have vaginas and appear female, have XY so no menstruating *sex assignment is female)
Fetuses at 8 weeks they look the same
Lordosis reflex concave arching of the back in response to a sexual mount (rodent species)
Question to ask 1. What did they (the experimenters) do? 2. Why did they do what they did? 3. What did they find? 4. What did they conclude? 5. What is the “bigger” question that is being asked and answered by the research?
MPN and gender difference between sexes bc of exposed to androgens during development (Males have more cells near their MPN compared to females)
Organizational effects happens early in development long lasting and irreversible
Testosterone helps develop van deferens , epididymis and vesicles
Activation effects happens later in life temporary and reversible
Congenital adrenal hyperplasia excessive production of androgens (testosterone) begin during fetal development CAH females have no significant development of wolffian duct structures No anti-mullerian ducts
Sex receptivity females depend on estrogen and progesterone and males depend on testosterone
Adrenal gland secrete ACTH (adrenocorticotropic hormone)
How are cortisol and aldosterone made? 21 hydroxylase (enzyme responsible for the conversion testosterone (CAH has a deficient in this enzyme)
Cortisol inhibits release of ACTH, that's why CAH happen (too many hormones, can't stop it when it's too much)
Sexual dimorphic nucleus between optic chasms cluster of cells related to sexual behavior (debated to relate to sexual orentation bigger in males continuous in males and cyclic in females
5 alpha reductase The enzyme responsible for the conversion of testosterone to dihydrotestosterone is
INAH3 (third interstitial nucleus of the anterior hypothalamus) humans SDN in humans Levay (1991): smaller in women, larger in men, homosexual men closer to women’s size Byne et al. (2001): results mixed
David Reimer (Diamond & Symondson, 1997) Botched circumcision → raised as girl Transitioned back to male in adulthood Takeaway: Socialization ≠ only factor in gender identity
Mice (Edwards, 1969) Injecting TP (testosterone propionate) on Day 1 vs Day 10 → different aggression outcomes Takeaway: Critical periods matter
Monkey Studies Prenatal testosterone → masculinized play (mounting, rough play) Early androgenized females (EAFs) vs Late (LAFs): EAFs: more male-like genitals, less rough play LAFs: female genitals, more rough play Takeaway: Behavior and anatomy can diverge
Sheep (Roselli et al.) Some rams = male-oriented OSDN (sexually dimorphic nucleus) size linked to orientation Prenatal testosterone timing changes OSDN size
BNST (Bed Nucleus of the Stria Terminalis) — Zhou & Swaab Larger in men than women MtF transgender brains resembled female pattern Suggests link to gender identity
Anterior Commissure (AC) — Allen & Sorski Larger in women + homosexual men vs heterosexual men
Amniocentesis sample amniotic fluid → test hormone exposure
Penile Strain Gauge (men) & Vaginal Photoplethysmograph (women) measures arousal
SDN location around tiny gap in bottom cross-section between optic chiasm
INAH3 location near SDN, symmetry one each side of gap
AC location above tiny gap in cross section of brain
BNST location on both sides of the AC above tiny gap
SDN meaning Sexual dimorphic nucleus
INAH3 meaning (third interstitial(in) nucleus of the anterior hypothalamus
AC meaning Anterior Commissure
BNST meaning Bed Nucleus of the Stria Terminalis
Pain/temp pathways small fibers → cross/ascend anterolateral → brainstem branches((pons medulla-arousal) → thalamus (VPL(Ventral posterolateral nucleus) & medial/intralaminar(inside)-->conscious (where)) → primary somatic sensory cortex(emotional/awareness)
Parts of a neuron dendrites (receive signals), soma (cell body), axon (sends signal), myelin sheath (insulates), axon terminals (release neurotransmitters), synapse (gap between neurons)
Resting potential Inside of neuron is negative relative to outside. Maintained by sodium-potassium pump (Na⁺ out, K⁺ in)
Depolarization Sodium (Na⁺) channels open → Na⁺ rushes in → inside becomes positive. All-or-nothing response → once threshold is reached, action potential fires.
Action potential Continuous electrical signal along axon Electrical signal converts to chemical signal at synapse
Refractory period K⁺ channels open → K⁺ moves out → inside becomes negative again (repolarization) Neuron temporarily cannot fire. Extra K⁺ outflow may cause hyperpolarization (even more negative than resting) Sodium-potassium pump restores original ion balance
Traveling through the neuron Action potential go to terminal Vesicles fuse w/ membrane, releasing neurotransmitters into synaptic cleft Neurotransmitters bind to receptors on next neuron If threshold is reached → new action potential in next neuron Cycle repeats (Na⁺ in, K⁺ out)
Myelin Sheath Fatty insulation around axon Action potentials jump between nodes of Ranvier Called saltatory conduction → makes signal faster
Sensory Information Pathway Contralateral processing: right side of body → left brain; left side of body → right brain
Skin receptors Touch sends signals to the spinal cord Ascend via dorsal column-medial lemniscus pathway Reach the thalamus Go to the somatosensory cortex
Affective touch comforting, caress touch
C-tactile fiber receptors to touch
Medial Lemnisci location line that goes up the spinal cord and into the thalamus on the right generally between SDN and VPN
VPN location In thalamus near the bottom on the right side in the curve of the brain
EPSP increase chance of action potential excitatory neurotransmitter
IPSP decrease chance of action potential inhibitory neurotransmitter
Proprioception The awareness of where your body parts are in relation to your other body parts
VPN meaning Ventral posterior nucleus
Love--Sternberg 1. Sexual desire 2. Limerence 3. Intimacy 4. Commitment
LV (lateral ventricle) location Above BnST on the right side of the cross section
Transduction Change to one signal to another signal
Intimacy State of closeness and connection with one or more person that makes you make safe and secure
Jankowiak & Fisher 1992 Found evidence of romantic love in 89% of cultures studied
SON super optic nucleus
PVN para ventricular nucleus (3rd ventricle, right of the small gap)
OT Oxytocin
VP Vasopressin
Buss et al, 1992 Measure: Electrodermal activity (skin conductance = arousal). Men show greater physiological and self-reported distress to sexual infidelity; women to emotional infidelity Men more arousal to sex inf, while women did to emotional inf
William et al, 1994--female no mating When given oxytocin in the lateral ventricle, females spent ~90 min with their partner vs. 30 min with a stranger, With just CSF, time with partner and stranger was the same (~30 min) → Oxytocin promotes pair bonding
Hualian & Insec, 1995--female mating CSF (control): P 90 min vs. S 30 min → strong bond. OTA (oxytocin antagonist): Partner = S(30 min each) → bond blocked. VPA (vasopressin antagonist): P90 min vs. S30 min → bond intact. → Oxytocin is necessary for female bonding
Winslow et al, 1993--male no mating CSF (control): Partner = Stranger (30% each). Oxytocin: Partner = Stranger (30% each). Vasopressin (VP) manipulation: Partner 100% vs. Stranger 30% → significant effect. → Vasopressin (not oxytocin) drives male bonding
Winslow et al, 1993 pt 2--male mating CSF (control): P100% vs. S30% → strong bond. OTA (oxytocin antagonist): P60% vs. S30% → bond weakened. VPA (vasopressin antagonist): P30% vs. S30% → bond blocked. → Vasopressin is essential for male bonding
OT and VP summary female bonding: oxytocin male bonding: vasopressin regardless of if they mated
Trust study Trust- when given OT investors gave more money to the trustee (trusting they will get money back) Risk- (make sure OT does not make ppl risk averse) OT and PL had same results, so not stat sig Could not replicate (even with MSC and NoC)
Olfactory pathway Odorants bind to receptors in the nose and send signals up to the glomeruli Then go through the mitral cells and are transmitted to high regions go the brain Go to lateral olfactory tract
LOT (lateral olfactory tract) location Bottom base of the brain on either side
Gustatory pathway Papilla-surface on tongue Taste buds on taste receptors, which travel through afferent axons Goes to thalamus then the medulla than the taste zone of the cortex (right side, amygdala, lateral hypothalamus, VPN or thalamus, primary gustatory cortex)
Taste Sweet Sour Bitter Salty Umami Fat
OFC Orbital frontal cortex
DMN(MDN) Dorsal medial nucleus of the thalamus
Shul, Slotnick, Duda, 1996 Rats and different liquids in tubes (taught to stop drinking after certain sol) Bi-both sides Uni-ofc one side Sham-non
Shuletae con’d’, 1996 Flavor detection: bi failed, rest pass Taste detection: all passed Oder detection: all passet
Created by: user-1973161
 

 



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