Biopsychology Exam 2 Study Guide
Biopsychology Exam 2 Study Guide 41363
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This 16 page Study Guide was uploaded by Jennifer Wagner on Monday October 17, 2016. The Study Guide belongs to 41363 at Kent State University taught by Dr. Douglas L. Delahanty in Fall 2016. Since its upload, it has received 36 views. For similar materials see Biopsychology in Psychology at Kent State University.
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Date Created: 10/17/16
Study Guide: Exam 2 Biopsychology 10/17/16 Vision: I. Vision and Perception a. Sensory transduction: the process by which sensory stimuli are transduced into receptor potential b. Sensory receptor: a specialized neuron that detects a particular stimuli II. Anatomy of the eye: responsible for eye movements; vergence: eyes move together; saccadic: eye movements that your eyes make to move from point of focus to point of focus as quickly as possible. Very jerky (evolutionarily important). Pursuit: can follow objects while moving A. Sclera—white part, skin, outer casing of the eyeball. Sensitive. Contains vitreous humor (liquid inside) B. Cornea—transparent shield. First point of focus, barely dials in, NOT focused in great detail. Bends and refracts light. C. Pupil—hole into the eye, surrounded by muscle (iris) D. Iris—muscle. Controls amount of light that can come into the eye. As you get older, gets worn out, difficult to adjust to light E. Lens—fine tuning and fine focus. Cataracts is the clouding of the lens. F. Retina—back of the eye. Transduction occurs here. How you go from a ray of light to the action potentials. If focusing too soon, near sighted, focused too late, far sighted. 1. First layer ganglion cells. Transparent, light passes. Neurons whose axons come together to make the optic nerve. Going further into the brain. (Back of the eye). 2. Second layer 3 types of interneuron cells a. amacrine—passing info perpendicularly. Good at perceiving edges with horizontal cells. b. horizontal cells—integrate all of the info in photoreceptors with amacrine cells. c. bipolar cells—connects and passes info along the path 3. Third layer photoreceptors duplexity theory. Doesn’t do anything until it hits this layer. a. rods responsible for vision in dim light: more sensitive: however, lack detail and color. First discovered when studying nocturnal animals who do not need to worry about seeing color. Sensitive to low intensity light. 120 million rods. High convergence: hundreds of cells down to one. b. cones vision in bright light finedetailed color. Maximally sensitive to one of three different wavelengths of light and hence encodes color vision. 6 million cones. Low convergence, close to 1 to 1 ratio between cone and ganglion, so precision and clearer images. G. Fovea high acuity vision. Indentation; area of highest visual acuity. Made up entirely of cones. Takes up 25% of the space used in the brain allocated for vision. No diluting of the lights, cells pulled out to the side so light directly hits the fovea. H. Optic nerve blind spot; optic disk I. Optic chiasma—crossover of axons carrying information. Vision is a contralateral sense based on field of vision (not by each eye). J. Lateral geniculate nucleus and then primary visual cortex—first synapse is on the lateral geniculate nucleus in the thalamus. First time light synapses. Very simple pathway. Retna, geniculate, striate (pathway). Geniculate nucleus has 6 layers of cells; inner two layers oldest evolutionary layers. Magnocellular layer: perception of form, movement, depth, and small differences in brightness. Need to know most basic human needs for survival. Outer 4 layers developed later, focus on fine detail, and color. How does light get transformed into neural signals? A. occurs in the photoreceptors: vision largely inhibitory process. Lamella: layer consists of photo pigments made up of other constituents. Rhodopsin: opsin found in rods. Light hits them and they bleach, retinal and opsin are separated. Sodium is coming in and needs energy. In dark, spending energy to keep receptors open. Sodium channels close when opsin and retinal split which closes the channel. Cell no longer depolarizing; it hyperpolarizes (gets less and less positive) so stops releasing glutamate. Bipolar and photoreceptor cells do not fire action potentials but release NTs on the ganglion cells which depolarizes the ganglion cells which are able to fire action potentials. Fire action potentials on the lateral geniculate in the thalamus then go to the striate cortex. Opsin and retinal join together to form a photo pigment. Constantly releasing glutamate (excitatory), inhibiting bipolar cell because vision is different, inhibitory process even though glutamate is typically excitatory. B. rods contain rhodopsin made up of opsin and retinal C. cones contain iodopsin (3 types) and photopsin Seeing edges A. Mach bands lateral inhibition. Show perceptually, see at more distinct level than what actually exists. B. Ganglion cells, lateral geniculate cells, and the lower layer of visual cortex cells are oncenter and offcenter cells most responsive to circular or curved edges C. Rest of visual cortex responds to straight edges (striate cortex cells) 1. simple cells respond best to bars—lines in certain orientation. Can’t move or inhibit it. must be in particular orientation and position 2. complex cells particular orientation but not position. Can move around but not pivot. Hyper complex cells fire at a higher rate when edges are seen. Important for detected straight edges. 3. Spatialfrequency theory cells respond even more to sine wave gratings then to straight edges. Combine different gratings and come up to something closer to what we actually see. Still take a big jump to what we actually see, more research needs to be done. Seeing color hues largely depends on the wavelength of light reflected off an object. Three types of photoreceptors. Red, blue, green. Blue has smallest number of cones (8%). 1. additive mixture each light adds its wavelength to the color mixture 2. subtractive mixture when you mix these colors they absorb more wavelengths or subtract that light from our vision Oncenter: if hit the center of the cell, then increased rate of firing, hits other parts, slows firing A. 2 main theories 1. trichromatic theory (YoungHelmholtz theory) Three types of receptors, each with a different spectral sensitivity. Works are photo receptor level. Can account for all different colors if you have red, green and blue cones. 2. opponentprocess theory Two different classes of cells encoding color and another class encoding brightness. Each encodes two opposite color perceptions. Red and green and yellow and blue. If you stare at one of these colors then a piece of paper, you see the opposite. Accounts for color afterimages and colors that cannot appear together (reddish green or bluish yellow). Work by the ganglion cell layer. Both theories right: coding of colors by cones seems to operate at the basic receptor level. From then on, opponentprocess theory is correct. Protanopia: first color deficit. Confusion with red and green cones. Red cones filled with green opsin. Sexlinked, more common in males. Deuteranopia: green cones are filled with red one opsin. Sexlinked. Common in males. Only have 1 X chromosome, so mother passes on gene. Tritanopia: an inherited form of defective color vision. Blue cones are either lacking or faulty. Can’t see blue, still can see clearly. Audition, Olfaction, Touch: A. What do we hear? Hear dimensions of sounds. Humans hear sounds within the range of 20 20,000 Hz (hertz = vibrations per second) B. cocktailparty phenomenon—there can be music, a conversation everywhere, a doorbell, a baby, and a dog and still hear your name being said and tune into what is being said. Audition: analytic sense. Can hear many different things and still understand and tune into them. Vision: synthetic. Adding everything together to create a whole. C. Three dimensions of sound 1. Loudness a function of intensity: Unit of measurement for loudness is decibels 2. Pitch determined by the frequency of vibration, measured in hertz (Hz) 3. Timbre nature of the sound/complexity. Very complex would be in an orchestra or other music. D. Anatomy of the ear 1. Pinna—outside of ear. Like a funnel to bring in more sound. 2. Auditory canal to the eardrum (tympanic membrane) which vibrates with the sound waves. Move with frequency, high frequency, faster movement of eardrum. 3. Ossicles (3 small bones of the middle ear) amplify sound waves as we go into a more liquid present location a. malleus (hammer) b. incus (anvil) c. stapes (stirrup) 4. the stapes rests on the oval window which is a membrane that is the beginning of the cochlea. Move from movement of vibrations to action potentials. Need 2 windows because cochlea is fluid filled. 5. cochlea snailshaped: contains the receptive organ organ of Corti: divided longitudinally into 3 fluidfilled canals a. hair cells receptor cells reside in basilar membrane, moves up and down. Highest frequency occurs at the top. Hair cells have axons that come together to form auditory nerve b. basilar membrane—very flexible, moves up and down depending on location of the frequency of the sound. As fluid moves past, cells bend and hairs move. Inner hair cells coding the cells. Outer hair cells in charge of keeping everything where it should be, more structural. c. tectorial membrane—very rigid d. round window Crossover occurs in the medulla in the superior olivary complex (part of the medulla) because contralateral. Inferior colliculus part of auditory pathway, then medial geniculate nucleus. Sent to auditory complex. E. From the ear to the brain very complex, the cochlea message is sent through the auditory nerve and hits the medulla and thalamus before going to the contralateral primary auditory cortex F. How do we hear? 1. Place coding evidence indicates that we hear moderate to high frequencies by place coding. Different frequency sounds stimulate different places on the cochlea. Bending hair cells in very specific spot, fire action potential accordingly. Different types of hair cells; inner hair cells help with actual hearing process. Lose higher frequency hearing first because hairs closest to basilar membrane become brittle. Cochlear implant has a wire that moves along the cochlear based on the frequency of cell. 2. Rate (Frequency) theory works best for low freq sounds. Tiny part vibrates. Tip link opens trap door when hairs bend; cations can go in. depolarizing the cells. G. How do we locate sounds? 1. arrival time and phase diffs—low frequency sounds. Hits one tympanic membrane before the other. Wave is coming in and hits one ear before other 2. phase diffs—low frequency sounds. Louder in one ear, before gets to next ear 3. intensity diff—high frequency sounds. IV. Taste Chemical senses: gustation (taste), smell. Hard to quantify taste and hard to do research Four basic qualities or types of taste sweet, sour, salty and bitter Recently added 5 taste: umami (meaty taste) Flavor, as opposed to taste, is a composite of olfaction and gustation. large differences in taste sensitivity as we age A. Anatomy of tongue 1. taste buds—ten thousand taste buds. Molecules must be dissolved by saliva in order to taste. Chemical particles fall into receptors. To taste salty, a substance must ionize. Sourness receptors respond to hydrogen ions. Bitter and sweet substances are difficult to characterize. 2. papillae visible protruberances on the tongue 3. hairlike processes in the space between papillae are stimulated and electrochemical signal occurs B. From tongue to brain 3 diff nerves carry taste info to brain goes through medulla and then to thalamus where it is routed to primary somatosensory cortex. Ipsilateral, not crossing over. Also goes to the hypothalamus and amygdala. V. Smell the other chemical sense humans have 10 mil smell receptors, different types smell is also very evocative—different smells trigger memories can be synthetic and analytic A. Anatomy of the nose 1. chemical molecules released from a substance are brought in through the nose and nasal cavity 2. olfactory epithelium where the olfactory receptors are contained 3. odorous molecules dissolve in mucous and stimulate receptor molecules, then stimulate G proteins 4. olfactory bulbs Go to limbic cortex and amygdala regions. B. How do we smell? 1. lockandkey theory different shaped receptors receptive to diff molecules, doesn’t work this way, we can smell a wider range of olfactions 2. Vibration theory molecules of distinct odor generate a specific vibration frequency in the nose. Different pattern of smells. Similarities between smells, go into subsection into similar smells. Vomeronasal organ—perfume, deodorant, pheromones. Other organisms completely guided by presence of pheromones. Ex) golden hamster, rats. For animals, entire reproduction and sexual behaviors related to Vomeronasal organ. Less important for humans. None of these are pleasant smells, one of the most repulsive smells. Use pheromone detection to be most attracted to certain mates and who will improve immune function in offspring Transduction of olfaction—can smell thousands of smells, so not lock and key. Instead, pattern of smells fall under each odorant that will bind to multiple receptors VI. Vestibular system A. Vestibular sacs head's orientation Utricle and Saccule. Used in telling where gravity is. Keeping upright. Otoconia—calcium carbonate bends hair cells, can tell what is up and what is down. Balance, maintenance of head in upright position, make sure eyes are focused B. Semicircular canals angular acceleration Three of them. Respond to angular acceleration. Changes in angular acceleration. Ampulla and inside of ampulla is cupula. You resist movement, so as you move, fluid moves through canal. Ampulla resists movement then moves a bit delayed. If you spin then fluid keeps moving and gets too revved up and you become dizzy. Vestibular pathway—synapse upon the cerebellum (movement info and smooth it out), spinal cord, medulla, pons, neck muscles, vestibule ocular reflex (to keep eyes focused as you move). If damaged, eyes move as body moves too much and cannot see as well, not as much focus while moving. VII. The somatosenses the sense of touch Proprioception and kinesthesia provide info about body position and movement. Critical for development and receiving information. A. Anatomy of skin 1. 2 types of skin a. hairy—every part of body that is not glabrous. Merkel’s disks not present here, all others found in hairy b. glabrous: more complex mixture of receptors—lips, palms, fingertips, balls of feet. Receptors respond to texture and manipulation and indentations. Ex) if holding remote and asked to name object without moving, very difficult. c. Pacinian corpuscles very sensitive to vibration—high concentration in glabrous d. Meissner's corpuscles & Merkel's respond to touch—more found in glabrous because of changes in pressure B. 3 distinct cutaneous (skin) senses 1. Touch pressure and vibration is caused by movement of the skin: when Pacinian corpuscle is bent, it depolarizes and fires 2. Temperature most agree that temp stimulates free nerve endings and that there are ones for heat and cold. Feelings of temp are not absolute, but relative. Relative to base environment. 3. Pain also associated with free nerve endings: evidence for chemical cause. Most psychologically mediated sense. Ex) soldiers shot 6 times, not even aware that they were shot until after. Some people pain sensitive, some pain resistant. Difficult to study pain because it is unethical to bring people into a lab and damage tissues. C. From skin to brain 2 (primary) pathways both coming into the dorsal side 1. Fast conducting: long myelinated axons that convey precisely localized info. touch or movement. Highly myelinated, dorsal columns: precise touch, not many synapses, nothing is diluted 2. Slow conducting: short unmyelinated axons that convey poorly localized info like pain and temp. Spinothalamic tract: dull, many synapses. D. pain perhaps one of the most psychologically mediated senses phantom limb pains. Have perceptions of pain. Central pain perception that the limb hurts even when amputated. Periaqueductal gray matter (PAG)—responsible for analgesia. Less perception of pain that needs to be involved in order to successfully reproduce or attempt of mating, so that we don’t say “ouch” and run away from need to mate. The biopsychology of eating and drinking: I. Eating Not meant to constantly have food presented and ability to eat all the time. A. We need to eat for 2 reasons: 1. construct and maintain our own organs (building) 2. obtain energy for muscular movement and warmth B. Shortterm storage cells in liver convert glucose to glycogen and store it: this process is stimulated by insulin: glucose levels fall, inhibit insulin and stimulate secretion of glucagon Glucose is primary fuel for the brain. In the liver we store 300 calories stored for use in the central nervous system. Convert glucose into glycogen when the pancreas secretes insulin. If the pancreas is not stimulated, it secretes glucagon and turns it into glucose. Glucose is not lipid soluble, need insulin in order to effectively transport glucose. C. Longterm storage fat (adipose tissue) stored more precisely as triglycerides. Broken into fatty acids and glycerol when needed to use to power the brain. Fatty acids can be directly used as energy in the muscles. Glycerol turned into glucose to power brain. D. Why do we start eating a meal? Used to be “I’m hungry” 1. Social and environmental factors More people around, eat more if others are eating. Studies with obese and nonobese individuals Some more externallycued rather than individually cued 2. Need for a variety of nutrients children / cafeteria diet Sensory specific satiety: sick of single food if we only eat similar taste. We will eat more if there are different flavors/tastes. Should be motivated to eat different things and consume different vitamins Conditioned taste aversion: most powerful pattern of learning. Eat something and get sick, then will not eat/drink that same thing for a long time after that 3. Depletion of nutrients A. homeostasis—eat when our stomach and upper intestine are empty. Emptiness provides a hunger signal. Ghrelin—a peptide hormone released by the stomach that increases and continues to increase until food in consumed, then levels drop. E. What stops a meal? 1. Oral cavity sham feeding studies Intragastric feeding 2. Stomach pylorus cuff. Stretch receptors activate and pull, signal to stop eating. 3. Small intestine cholecystokinin (CCK) is a hormone secreted by the duodenum that regulates gastric motility and causes the gallbladder to contract; appears to provide a satiety signal transmitted to the brain through the vagus nerve. Also PYY is released to tell you to stop eating. F. Connections between stomach and brain Longterm satiety: signals from adipose tissue More adipose cells wanting to be full. When adipose sites full, release leptin (hormone secreted by adipose tissue) that shuts down eating. Many studies in animals (mice) showed this to be effective. Not successful or as clear in humans. 1. Neural mechs vagus nerve 2. Calories signaled by nonneural means G. Neural mechanisms of eating 1. Two areas of the hypothalamus the lateral hypo and the vetromedial hypo (VMH): a. lateral hypo "hunger center" b. VMH "satiety center" paraventricular nucleus. II. Drinking behaviors A. drink to maintain body's fluid levels two responses to water deficits 1. drink 2. vasopressin diabetes insipidus, not enough vasopressin, cannot drink enough to satisfy, always thirsty. Hypothalamus tells pituitary to release vasopressin B. fluid levels must be maintained in four fluid compartments in the body 1. intracellular (70%) fluid portion of cytoplasm. Most important because our cells are dependent on fluid and need to be hydrated 2. interstitial (26%) – fluid bathing all cells of the body 3. intravascular – in blood vessels. Also very important so there is movement of blood 4. CSF C. isotonic concentration of solutes in neighboring compartments is relatively the same Hypertonicgreater concentration of salt, solutes Hypotonic –less solutes, more fluids Water moves from lowest solute concentration to highest solute concentration. Solutes do not move, the water is what moves to the hypertonic sections. D. 2 types of thirst 1. Osmometric – ingesting salt causes this. Occurs when tonicity of interstitial fluid increases: osmoreceptors is a cell that when losing fluid, fires faster in the anteroventral third ventricle (AV3V) and the OVLT lesions to these areas result in no longer drinking 2. Volumetric occurs when volume of blood decreases. Need to replace what we note as a drop in blood volume. Renin, which enters blood and converts angiotensinogen to angiotensin: also receptors located in the heart that can stimulate thirst: subfornical organ Angiotensin 2: Retention of sodium, stimulates pituitary to release ADH and retention of water (osmometric thirst), increase blood pressure, stimulates adrenal glands to release aldosterone retain salt (osmometric thirst), stimulates drinking and salt appetite (OVLT) Sexual Development: I. Defining males and females Sexually dimorphic behaviordifferent forms of different behavior in males and females II. Sexual development A. Fertilization XY (Male) vs XX (Female), sperm, egg or ova called gametes Sexually dimorphic behavior: differs by sex. Parts of behaviors or parts that differ between males and females. III. Development of sex organs 3 general types of sex organs A. Gonads develop first: testes and ovaries. Fertilization is first pathways to developing as either male or female. 6 weeks gonads start forming. SRY gene (on Y chromosome) secretes testis determining factor (TDF) which leads to the development of testes. If you don’t have an SRY gene, ovaries develop by default. Females develop unless something different happens. 3 months is when internal sex organs begin forming. Everyone has precursor to both female (Muellerian) and male (Wolffian) internal sex organs. For males, testes secrete testosterone which triggers development of Wolffian system and anti Mullerian Hormone. Testosterone releases masculine effect; triggers Wolffian system to start. Anti Mullerian Hormone triggers drying up of Mullerian system. (Androgen is combination of all different kinds of male sex hormones.) Testosterone leads to development of external organs, for females, since there is none, then vagina forms. For females, there is not anti Mullerian system, and no testosterone that triggers masculinizing effects, so ovaries are produced. Persistent Mullerian duct syndrome—A condition caused by a congenital lack of anti Mullerian hormone of receptors for this hormone; in a male, causes development of both male and female internal sex organs. Turner’s syndrome will develop external female genitalia, not internal so sterile. Castration—either removing testes or ovaries. Orchidectomy—remove testes Ovariectomy—remove ovaries 1. SRY produces an enzyme called testisdetermining factor which stimulates the undifferentiated gonads to develop into testes B. Internal sex organs Fallopian tubes, uterus and vagina in female and epididymis, vas deferens, seminal vessicles and prostate in men 1. Wolffian system (male) and a Mullerian system (female) 2. Testes secrete testosterone and Mullerian inhibiting substance: masculinizing and defeminizing Estrogen is responsible for masculinizing brain Aromatization – converts androgens into estrogen. Alphafetoproteins destroy estrogen in bloodstream. Testosterone can pass, goes into brain. Estrogen cannot cross blood brain barrier due to alphafetoproteins Estrogen is present in male brain because testosterone in brain is changed into estrogen and masculinizes brain Organizational effect—(of hormone) the effect of a hormone on tissue differentiation and development. Making tissues and secondary sexual characteristics Activational effect—(of hormone) critical time for development differentiation. The point where you can generate gametes. Using sperm and making eggs. C. External genitalia 1. External reproductive organs penis and scrotum in males: labia, clitoris outer part of vagina in females a. bipotential precursor b. development of external genitalia also controlled by the presence or absence of testosterone IV. Sexual maturation – puberty. Primary sex characteristics include the gonads, internal sex organs, and external genitalia. These organs are present at birth. Secondary characteristics include, development of breasts, pubic hair, deepening of voice, widening of hips. A. Gonads are controlled by the pituitary which is in turn controlled by the hypothalamus 1. Gonadotropin releasing hormone (GnRH) which reaches the anterior pituitary which stimulates gonadotropins (Folliclestimulating hormone, FSH and luteinizing hormone, LH) released in both males and females which reaches the gonads and causes release of the gonadal hormones androgens, estrogens and progesterones Hypothalamus releases gonadotropinreleasing hormone that releases gonadotropin. Adrenal cortex is other place that releases testosterone, estrogen, and progesterones Estrogens and androgens present in both sexes, but the amounts differ. 2. Androgens – testosterone. Responsible for hair growth. Secondary sex characteristics in males. 3. Estrogens estradiol result in development of secondary characteristics in women 4. Female gonadal hormone levels are cyclic males are steady V. Gonadal hormones effects on adults Activation effects in males: A. Orchidectomized males—remove testes in adulthood, leads to drop in sexual behavior but to a varying degree. Due to preexisting activity. If you increase testosterone, don’t have an increased appetite for sex. B. Coolidge effect—the restorative effect of introducing a new female sex partner to a male that has apparently become “exhausted” by sexual activity. Male have shorter refractory periods if new partner is introduced. Coined by President Coolidge visiting a chicken farm with only a few roosters. Activational effects in females: Estradiol and progesterone. Women most likely to initiate during high levels of estradiol and testosterone. Levels of gonadal hormones: in males, steady state, in females, cyclical due to differences in the hypothalamus C. Male and female sex behavior VI. Exceptions to the rule A. Androgenic insensitivity syndromeThe body doesn’t recognize the presence of androgens at all. Has testes but no internal female sexual organs, no external male genitalia. No ovaries or menstrual cycle. No pubic hair due to absence of androgens. Testes and adrenal cortex release estrogen, responsible for puberty and appearing as a female due to secondary sex characteristics. Remove testes because when impacted can be cancerous. Can elongate vagina, but could not have children because no ovaries present. B. Andrenogenital syndrome (congenital adrenal hyperplasia)adrenal glands pump out high levels of androgens, testosterone. Find that in males it doesn’t matter—go into puberty early. In females, varying levels of testosterone but doesn’t occur early enough to impact internal female sex organs. Impact on external genetalia. Results in enlarged clitoris and fused labia. Can be surgically corrected. See much higher rate of homosexuality (over 40%) report being lesbian. C. Penile ablation – Money—identical twin names Bruce. At 8 months had boys circumcised, went horribly wrong and burnt off Bruce’s penis. Money was the leading sex researcher in the world. Believed in nurture only, not nature. How you are parented. Suggested to raise Bruce as “Brenda” with hormone injections and female genetalia. Followed twins for years, said Brenda developed into “normal” female. Came out that he minimized all study results, committed fraud. Comes out as “David” and said she never felt female and didn’t want to be a female. Took steps to turn back into a male. VII. Brain differences—females tend to use both hemispheres more than males do who typically use only one. A. Hypothalamus—very different. Males: steady, females: cyclic 1. Sexually dimorphic nuclei—larger in males (5 times larger than in females). 2. Medial preoptic area of hypo—essential area for males. Rostral to hypothalamus. If you destroy it, you destroy sexual behavior. Does not destroy sexual behavior in females. 3. Ventral medial hypothalamus—parallel area for sexual area in females. If lesion the VMH then decrease sexual behavior in females VIII. Sexual preference A. sexual preference has nothing to do with hormone levels Small subgroup of lesbian women who have higher than normal levels of testosterone (30%). Could be lifestyle based, born, but not significant. B. brain differences Prenatal exposure to androgens can impact sexual orientation. Higher rates of homosexuality for females when introduced to testosterone early in development. Stress levels reduce release of testosterone/change level of androgens. Also, largely genetic. More older brothers you have, more likely last child would be homosexual (use up/used to testosterone). Look at concordance rates in identical twins versus fraternal twins. 1. 3rd interstitial nucleus of the anterior hypothalamus (INAH 3)
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