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Behavioral Neuroscience Chapter Notes.docx

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PSYC 3410
Elena Choleris

Behavioral Neuroscience Chapter Notes Chapter 13 – Hormones and Sex Mamawawa: Men are Men and Women are Women assumption: the tendency to think about femaleness and maleness as discrete, mutually exclusive, opposite categories – this assumption seems right but it is fundamentally flawed - In thinking about hormones and sex : assumption is females have female sex hormones that give them female bodies and make them do female things. And vice versa for men. Developmental and Activational Effects of Sex Hormones Hormones influence sex in two different ways: 1) By influencing the development from conception to sexual maturity of the anatomical, physiological, and behavioral characteristics that distinguish females vs. males 2) By activating the reproduction-related behavior of sexually mature adults Neuroendocrine System - Endocrine glands: are organs who’s primary function is to release hormones - Note: some other organs i.e.: stomach, liver, intestine and body fat also release hormones into general circulation and are therefore also part of the endocrine system. Glands 1) Exocrine Glands: (eg sweat glands) release chemicals into ducts which carry them to their targets. Mostly on surface of the body 2) Endocrine Glands: (ductless glands) release their chemicals, called hormones, directly into the circulatory system. Once in the circulatory system, the hormone travels until it reaches its target. Gonads - Gonads are in males: testes and in females: ovaries. = sperm and egg production - Copulation (intercourse) = one egg and one sperm meeting to form a Zygote. - Zygote: contains all information necessary for normal growth of complete organism - Each cell of human body = 23 chromosomes. Egg and sperm = half in order to create a whole when they come together. They contain Sex Chromosomes (which contain genetic information) - Females = XX - Males = XY - Half of the sperm cells have an X and half of the sperm cells have a Y chromosome Classes of Hormones Vertebrate Hormones fall into three classes 1) Amino acid derivative: hormones that are synthesized in a few simple steps from an amino acid molecule Ex. Epinephrine: released from adrenal gland and synthesized from tyrosine 2) Peptides and proteins: chains of amino acids, peptide hormones = short chains; protein hormones = long chains 3) Steroids: hormones that are synthesized from cholesterol , a type of fat molecule - Hormones that influence sexual development = STEROIDS - Steroids: bind to receptors in cell membranes and can influence the cells and their gene expression. They are small and fat soluble. – they have the most diverse and long lasting effects on cellular function. Sex Steroids Gonads also release steroid hormone Two Main classes of Gonadal Hormones: 1) Androgens: testosterone is the most common one 2) Estrogens: estradiol is the most common one - Ovaries produce more Estrogens that Androgens and Testes vice versa 3) Progestins: progesterone is the most commone - This hormone is also released from the ovaries and testes in men and woman. o Its function in men unclear BUT in woman prepares uterus and breasts for pregnancy - Adrenal Glands (although not a primary sex organ) also releases all three of these hormones. Hormones of the Pituitary Gland - Pituitary Gland: frequently referred to as the master gland because most of its hormones are tropic hormones (hormones whose primary function is to influence the release of hormones from other glands) - Example: Gonadotropin is the pituitary hormone that travels through circulatory system to the gonads to stimulate release of gonadal hormones - Anterior and Posterior pituitary gland are fused together o Posterior gland: develops from small outgrowth of hypothalamic tissue and dangles at the end of the Pituitary Stalk o Anterior gland: begins as the same tissue and develops into the roof od the mouth and during the course of development migrates upwards and rests beside the posterior pituitary. Anterior pituitary releases the Tropic Hormones* Female Gonadal Hormone Levels Are Cyclic; Male Gonadal Hormones Are Steady - Although woman and men possess the same hormones they are not present at the same levels and do not necessarily perform the same function - Females: Menstrual Cycle: controlled by regular hormone fluctuations - Males: gonadal and gonadal tropic hormones change very little day to day Study by Geoffrey Harris (1977) - Cycling pituitary removed from female rat - Became steady state pituitary when transplanted into a male - A steady state pituitary removed from male - Became a cycling pituitary when transplanted in female - Therefore anterior pituitaries aren’t inherently female (cyclic) or male (steady), their patterns of hormone release are controlled by another part of the body Neural Control of the Pituitary Gland - Nervous system was implicated the control of the anterior pituitary gland due to the behavioral research on birds and other animals that breed only at specific times of the year o Seasonal variation in light-dark cycle triggered breeding related changes in hormonal release o Visual input to the nervous system was controlling the release of tropic hormones. - The pituitary system is therefore controlled by the HYPOTHALAMUS o Mystery is that the posterior pituitary was the only part of the gland that had connection with the hypothalamus, not the anterior gland which is associated with the tropic hormones. Control of the Anterior and Posterior pituitary by the Hypothalamus - Two different mechanisms by which the hypothalamus controls the pituitary; one for posterior and one for the anterior o Two major hormones of Posterior pituitary = vasopressin ( facilitates reabsorption of water in the kidenys) and oxytocin (stimulates contraction of uterus in labor and ejection of milk during suckling)  They are peptide hormones synthesized in cell bodies of neurons in paraventricular nuclei and supraoptic nuclei on each side of the hypothalamus  They are then transported down axons and wait in the posterior pituitary  When action potential occurs they are released into the bloodstream (neurosecretory cells) o Hypothalamopituiray Portal System: network of hypothalamic capillaries feeds a bundle of portal veins that carry blood down the pituitary stalk into another network of capillaries in the anterior pituitary gland o If the portal veins are cut the release of anterior pituitary hormones are disrupted until veins regenerate Discovery of Hypothalmic Releasing Hormones Hypothesized: - Releasing Hormone: hypothalamic hormones thought to stimulate release of anterior pituitary hormones - Release- Inhibitory Hormone: hormones that inhibited the release Breakthrough: (1960’s Guillemin and Schally) - Thyrotropin- releasing hormone found in sheep and pigs o This releasing hormone (in hypothalamus) releases thyrotropin from anterior pituitary gland (APG) which in turn stimulates release of hormones from thyroid. - Gonadotropin-releasing hormone (Schally): this releasing hormone stimulate release of both anterior pituitary gonadotropin hormones o Follicle stimulating hormone (FSH) o Luteinizing hormone (LH) Regulation of Hormone levels - Hormone release regulated by: o Signals from the nervous system  All endocrine glands except anterior pituitary are directly regulated by signals of the nervous system  Endocrine glands in brain : pituitary and pineal – are regulated by cerebral neurons  Innervated by autonomic system : sympathetic or parasympathetic (each having opposite effects on hormones)  Hormone release regulated by experience o Signals from hormones  Tropic hormones release other hormones  There are also circulating hormones that turn off the pituitary and hypothalamus and other brain sites  Hormone feedback – maintenance of stable blood and hormones o Signals from non-hormonal chemicals in the blood  Glucose, calcium, and sodium levels in blood all influence the release of particular hormones  Ex. insulin and blood glucose levels Pulsatile Hormone Release - Hormones tend to be released in pulses (few minutes at a time but pulse frequency can change) - Large minute to minute fluctuations in levels of circulating hormones Summary Model of Gonadal Endocrine Regulation - Brain controls release of gonadotropin-releasing hormones from hypothalamus into hypothalmopituitary portal which carries it to the anterior pituitary gland - In the APG the gonadotropin-releasing hormone releases gonadotropin which is carried by circulatory system to the gonads - Gonads then release androgens, estrogens, and progestin - Which then feedback back to pituitary and hypothalamus Hormones and Sexual Development of the Body - Humans are dimorphic (two standard models = male vs female Fetal Hormones and Development of Reproductive Organs - Primordial Gonads (6 weeks after fertilization) female and male look the same o Cortex (outer covering) - potential to grow into ovary o Medulla – potential to grow into testis - Sry gene (on Y chromosome) triggers synthesis of Sry protein which causes medulla to grow into testis (6 weeks after conception) - Absence of Sry protein = ovaries grow - If the Sry protein is injected into female fetus, the female will grow with testes - If Sry protein is blocked in male fetus, male will have ovaries Internal Reproductive Ducts - Wolffian System (male) – has capacity to form seminal vesicle - Mullerian System (female) – has capacity to form uterus and fallopian tubes - Mullerian Inhibiting Substance is secreted by testes which causes Wolffian system to take over and scrotum to develop (third month of fetal development – male) – females who are injected with this substance at the appropriate time in development grow both ducts - Ovariectomy: removal of ovaries - Orchidectomy: removal of testes - Gonadectomy: surgical removal of gonads (castration) External Reproductive Organs - Both male and female genitals develop from the same precursor (bipotential precursor) - 2 month of pregnancy = glans, urethral folds, lateral bodies, labioscrotal swellings o Then they begin to differential  Glans = head of the penis OR clitoris  Urethral Folds = fuse in the male OR become labia minora  Lateral Bodies = shaft of penis OR hood of clitoris  Labioscrotal swellings = scrotum OR labia majora o All controlled by the presence or absence of testosterone Puberty: Hormones and Development of Secondary Sex Characteristics - Puberty: the transitional period between childhood and adulthood during which fertility is achieved , adolescent growth spurt occurs, and secondary sex characteristics develop - Puberty is associated with increase in release of hormones from APG - Growth Hormone released : is the only hormone not targeted at a gland and targets the bone and muscle tissue - Gonadotropic and adrenocorticotropic hormones cause gonads and adrenal glands to increase release of gonadal and adrenal hormones = maturation of sex organs and secondary ones - Pubertal Males = higher androgens - Pubertal females = higher estrogen - Individuals that have been castrated do not have this growth unless injected with androgens or estrogens or given the missing part - Androstenedione initiates pubic growth and underarm hair growth (axillary) in both sexes (IS an Androgen) - Pubic Hair : Male pattern = pyramid Female pattern= inverted pyramid - Puberty Begins : Males = 11.5 Females = 10.5 o Dietary, Socioeconomic, and Medical care = lowered age in puberty Sex Difference in the Brain - Men = 15% larger brain - Differences in the volumes of various nuclei and fiber tracts, neural and glial cells, number of synapses… - Sexual Dimorphisms (male and female structures differ) First Discovery of a Sex Difference in Mammalian Brain Function - Seminal Experiments by Pfeiffer (1936) o Used neonatal rats (males and females) o Some gonadectomized and some not o Some received gonad transplant and some did not (ovaries or testes)  FOUND : gonadectomizing neonatal rats of either sex caused them to develop into female cyclic patterns  Transplantation of testes into gonadectomized or intact female neonatal rats caused them to develop into adults with male patterns of gonadotropin release  Transplant of ovaries had no effect on hormone release  Therefore: female cyclic pattern develops unless female cyclicity is overridden by male testosterone during prenatal development o We know now: the release of gonadotropins from the APG is controlled by hypothalamus - Aromatization Hypothesis: o Aromatization: all gonadal and adrenal sex hormones are steroid hormones (cholesterol) therefore they have similar structures and are easily converted from one to another. o Aromatization Hypothesis: prenatal testosterone does not directly masculinize the brain; brain masculinized by estradiol  weird considering ‘female hormone’ (a changed testosterone from the enzyme = aromatase) the change occurs in the brain o Evidence 1) masculinizing of the brain from injections of estradiol 2) masculinization of the brain does not occur with testosterone o Alpha fetoprotein: present in the blood of rats during perinatal period and deactivates circulating estradiol by binding to it (how females don’t have masculinized brain) o Testosterone is not effected by alpha fetoprotein therefore when testosterone in the brain changes it estradiol male isn’t affected because the alpha fetoprotein can’t go past blood brain barrier. AND women don’t have testosterone. - Modern Perspectives on Sexual Differentiation of Mammalian Brains o Aromatase only found in specific areas of the brain (hypothalamus) o Aromatization is different in species: less prominent role in primates than rats and mice o Many differences in the brain do not develop until puberty o Sex chromosomes found to influence brain development independent of their effect on hormones o Female brain needs estradiol for some parts of development o **Although the conventional view that a female program of the development is the default does an excellent job of explaining differentiation of the reproductive organs, it FALTERS when it comes to differentiation of the brain** Perinatal Hormones and Behavioral Development - Phoenix and colleagues (1959) o Discovered prenatal injection of testosterone masculinizes and defeminizes a genetic female adult copulatory behavior.  Did experiment on female guinea pigs and ovariectomized and injected testosterone (females displayed male copulating behavior) BUT when re injected with progesterone and estradiol and were mounted they displayed less LORDOSIS - Grady Phoenix and Young (1965) o Lack of early exposure to testosterone in male rats feminizes and de masculinizes male adult rat copulatory behavior (intromission, mounting and ejaculation)  were castrated o Aromatization important for masculinizing and defeminizing (not in monkeys) o Injecting testosterone in rats for most masculinization critical in first 11 days of birth o We know less about role of hormones on Proceptive Behaviors (solicitation) vs. copulatory behaviors  BUT perinatal testosterone has been reported to disrupt proceptive hopping, darting, ear wiggling of receptive female rats; increase aggressiveness in female mice; decrease maternal behavior in female rats; and increase rough social play in female monkeys and rats. - Cohen-Bendahan, van de Beek, and Berenbaum (2005) o (despite inconsistencies) – prenatal androgen exposure contributes to the differences in interests, spatial ability, and aggressiveness typically observed between males and females - Notes some female behaviors observed in males (lordosis) and some male behaviors associated in females (mounting – Lucy) Three Cases of Exceptional Human Development Case of Anne S, the Woman who wasn’t. - Lack of menstruation and pain when having sex - Could not have children - Had peculiar pubic and axial hair growth (sparse and fine) - Externally she was normal BUT her vagina was only 4 cm long and her uterus underdeveloped - Her sex chromosomes were those of a male o Scraped mouth revealed XY o Internalized testes but no ovaries o Hormones of a male - Androgenic Insensitivity Syndrome: mutation of the androgen receptor gene (made them unresponsive)  body did not respond to male hormones in her system. Therefore = external genitalia and brain development and behavior as female. Mullerian inhibiting system was triggered which is why her male genitals did not develop o Her gender identity, sexual orientation, interests, and cognitive abilities were all still female The Case of the Little Girl Who Grew into a Boy - “Elaine” (1972) had ambiguous external genitalia - Raised as a female - Hit puberty and grew male secondary sec characteristics - Surgery to widen vagina and to clip the elongated clitoris - Hormones taken to suppress androgen release so that estrogen could feminize her - Had husky voice and narrow hips BUT grew up as a woman - Andrenogenital Syndrome: caused by congenital adrenal hyperplasia - a congenital deficiency in the release of the hormone cortisol from adrenal cortex = compensatory adrenal hyperactivity and excessive adrenal androgens o For males it only accelerates puberty o Females = large clitoris and fused labia. Internal organs are okay  Usually diagnosed at birth and therefore get surgery and cortical administration  Late menstruation  Tend to be tomboys, stronger, and aggression  Increased tendency for homosexuality  In 1950 children were left to grow up and let their bodies decide what they were going to be (very emotional because some grew up as men and grew female parts and vice versa) The Case of the Twin who Lost His Penis - Males penis destroyed in circumcision at 7 months - John Money recommended castration, artificial vagina, estrogen administered at puberty, and raised as female - Ablatio Penis - Ultimate test of Nature vs Nurture - When patient was 12 ‘she’ had developed as normal girl - BUT follow up study (Diamond and Sigmundson 1997) o Despite female genitalia and being treated as female John/Joan developed along male lines o Brain developed as a male o She eventually switched to become a male at 14 o He lived happy male life o Later committed suicide Do Exceptional Cases Prove the Rules? - These cases Contributed greatly to sexual differentiation of the body BUT still does not supply all answers about the brain development Effects of Gonadal Hormones on Adults Male Reproduction Related Behavior - Bremer(1959) o Important role of gonadal hormone in the activation of male sexual behavior demonstrated by the asexualizing effects of orchidectomy o In his experiment of orchidectomized patients many of which had committed sex related offences and did this to reduce sentence  Orchidectomy = removal of pair glands that release many hormones, most importantly testosterone = reduction in sexual interest and behavior  But rate and degree of loss are variable  Half of the men became completely asexual  Others lost ability of erection and copulation  Few had sex drive  Reduced body and facial hair, and fat deposited to the hips, and softening of skin  Some men kept sex drive due to adrenal androgens ?  Out od 102 sex offenders 3 recommitted  Therapeutic effects = replacement injections of testosterone - The Case of the Man Who Lost and Regained His Manhood o War veteran castrated by shrapnel (removed testes but not penis o He developed soft skin, lost muscle tone, narrowed shoulders and widened hips o No erection o Given injections of testosterone and was able to regain body mass and get erections again - Facts of testosterone o INCORRECT ASSUMPTIONS: 1) level of man’s sexuality is dependent on testosterone in blood 2) sex drive can be increased by increasing testosterone levels o Sex drive and testosterone levels are uncorrelated - Grunt and Young (1952) o Rate sexual behavior of male guinea pigs o Then divided the pigs into three groups : low, medium and high sex drive o All casterated = all sex drive dropped o When given testosterone injections it recovered o ** although each pig got same injection levels all the guinea pigs went back to their old sex drive levels - Davidson, Kwan and Greenleaf (1982) o Dihydrotestosterone = a nonaromatizable androgen restores the copulatory behavior of castrated male primates BUT not rodents  different systems Female Reproduction-Related Behavior and Gonadal Hormones - Sexually mature female rats and guinea pigs = 4 day cycles of gonadal hormone release o Gradual increase in secretion of estrogen by developing follicle 2 days prior to ovulation followed by sudden surge of progesterone as egg released o Surges of estrogen and progesterone = Estrus – a period of 12 to 18 hours where female is fertile and receptive (lordosis will occure) perceptive (behave in ways to get male attention) and sexually attractive (smelling of chemicals that attract male o Estrus cycle = cycle of sexual receptivity – has close relation with cycle of hormones o Ovariectomy = decline in receptive and proceptive behaviors  Estrus cycle can be induced by estradiol injection followed by progesterone injectioin o Female primate are only mammal motivated to copulate during non-fertility  Ovariectomy has little effect on their motivation to do this  But it does have effect on sterility and vaginal lubrication o Some studies indicate menstrual cycle associated with sex drive  But other contradicting studies have been held o Some studies support female sex drive comes from androgens (not estrogen) :  Experiment with female primate – injection of testosterone and not estradiol increased proceptivity of ovariectomized and adrenalectomized monkeys  Correlated studies of healthy women= sexual modivation correlates with testosterone levels but not with estradiol  Woman with ovariectomy and adrenalectomy or menopause had injections of testosterone that increased their sex motivation o Testosterone skin patch for low sex driven women  not proven that it will help. Because women with low sex drives don’t have low blood testosterone levels o Women prefer more masculine faces on fertile days that non-fertile Anabolic Steroid Abuse - Anabolic Steroids: steroids, such as testosterone, that have anabolic (growth promoting) effects. - Testosterone by itself is not used because it is broken down soon after injection because of undesirable effects o Chemists have created anabolic steroids that are long-acting BUT they do have side effects - Anabolic steroids are used in bodybuilding, competitive athletes, and in cosmetics o Very overused and abused Effects of Anabolic Steroids on Athletic Performance - Affect of anabolic steroids is inconsistent in whether they increase muscularity and strength - Failure of knowing the benefits is due to : o Experiments use small doses and for shorter periods o Experiments were used on participants that were not involved in as intense training o BUT some has been successful Physiological effects of Anabolic Steroids - Male Negative Side Effects from Use: o Reduction in gonadotropin release o Reduction in testicular activity o Testicular atrophy (wasting away of testes) o Sterility o Gynecomastia (breast growth)  from aromatization of anabolic steroids to estrogens - Woman Negative Side Effects from Use: o Amenorrhea (cessation of menstruation) o Sterility o Hirsutism (excessive growth of body hair) o Growth of clitoris o Masculine body shape o Baldness o Shrinking of breasts o Deepening of voice o Some effects are irreversible - Male and women who use anabolics can suffer from muscle spasms, muscle pain, blood in urine, acne, general swelling from water retention, bleeding of tongue, nausea, vomiting, and variety of psychotic behaviors; fits of depression and anger - Oral anabolics produce cancerous liver tumors - Bronson & Matherne (1997) o Experiment on male mice taking 4 types of anabolics at doses relative to humans. – no mice died BUT o At 20 months of age (6 months after experiement)  52% died while control mice 12% died - Two general health concerns: o Use of anabolics before puberty = risky in development o Many of the side effects take years to be manifested  May not pay the price now, but can later in life Behavioral Effects of Anabolic Steroids - Suggestions that anabolics increase aggression and sexual behaviors o Because belief of testosterone causes aggression  reports of aggression in steroid users may be consequence of expectation o Many who use steroids (aka in football players or fighters) may have been aggressive before o Aggressive behavior may be indirect consequence of increased size and masculinity - Pope, Kouri, and Hudson (2000) o Injected testosterone or placebo in double blind study of 35 men  Each individual rated aggression and kept diary of their aggressive levels  Increase in aggression was only found in a few volunteers - No evidence that it will increase sex drive - Studies have shown on male and female rodents that copulatory behavior is increased when on steroids - And anabolics have said to have an effect on copulatory behavior in males Neuroprotective Effects of Estradiol - Estradiol can reduce the brain damage associated with stroke and various neurodegenerative disorders - Yang and Colleagues (2003) o Estradiol administered to rats just before, during, or just after cerebral hypoxia (reduced oxygen to brain) reduced subsequent brain damage - Neuroprotective properties: o Reduce inflammation, encourage axonal regeneration, promote synaptogenesis, increase adult neurogenesis, increases survival rates of new neurons - Estradiol MAY: Increase women’s longevity, and lower their incidence of common neuropsychological disorders such as Parkinson’s. May explain decline in memory in post menopause - Suggestions for improving effectiveness of estradiol therapy: o Sherwin (2007) – not that success in humans and nonhumans is when administration is at menopause or shorty after o Marriot and Wenk (2004) – recommending smaller doses that mimic natural cycle of estradiol levels Natural Mechanisms of Sexual Behavior Structural Differences in Male and Female Hypothalamus - Functionally different in their control of the anterior pituitary gland hormones (steady vs. cyclic) - Raisman & Field (1971) o Structural difference in hypothalamus in rats - Gorski and colleagues (1978) o Discovered nucleus in medial preoptic area of rat hypothalamus that was larger in males o Nucleus = Sexually dimorphic nucleus o At birth nucleus were the same size but after a few days males grew at a higher rate o Growth was due to Estradiol o Castrating day old (not 4 day old) male rats = reduces size of the nuclei in adults . And administrating neonatal injections of testosterone increases size in adult female’s nuclei o Size of male rats SD nucleus correlated to testosterone levels and aspects of sexual activity o Specific function of nucleus is unclear o Further research shows there is dimorphism in nuclei in preoptic, suprachiasmatic, and anterior regions of the hypothalamus Hypothalamus and Male Sexual Behavior - Medial Preoptic Area (including SD nucleus) = area of hypothalamus with key role in male sexual behavior o Destruction of this area destroys male sexual behavior in all mammalian species o Lesions to this area in females do not destroy their sexual behaviors BUT do remove their male sexual behaviors that they sometimes exhibit o Therefore damage to this area abolishes male copulatory in both sexes o Medial Preoptic circuits appear to be dopaminergic o Medial Preoptic Area = involved in motivational aspects of male sexual behavior  Via a tract that connects to lateral tegmental field (midbrain)  destruction of this tract disrupts male sexual behavior  Activity in neurons of Lateral tegmental field of rats correlates with aspects of the copulatory act Hypothalamus and Female Sexual Behavior - Ventromedial Nucleus (VMN) of rat hypothalamus seem to be critical in female rat sexual behavior o Female rats with bilateral lesions of VMN do not display lordosis and have tendency to attack suitors o VMN and surrounding areas have a large number of progesterone receptors  Therefore VMN has role in Estrus o VMN on Sexual Behavior of female rats is mediated by tract that descends to periaqueductal gray (PAG) of tegmentum  destruction or lesions in tract destroy sexual behavior in females Sexual Orientation and Sexual Identity - Heterosexual (opposite sex attraction) vs. Homosexual (same sex attraction) vs. Bisexual (attracted to both sexes) - Sexual Identity: the sex, male or female, that a person believes him or herself to be. Sexual Orientation and Genes - Differences in sexual orientation have genetic basis - Bailey and Pillard (1991) o 52% of monozygotic twin brothers were homosexual o 22% of dizygotic twin brothers were homosexual o 48% of monozygotic twin sisters homosexual o 16% of dizygotic twin sisters homosexual o Gene for male homosexuality located on X chromosome  but lots of research have not confirmed this claim Sexual Orientation and Early Humans - Myth : homosexuals have lower number of sex hormones  incorrect homo and hetero do not differ - Orchidectomy = reduce sexual behavior in both homo and hetero males and when replacement injections occurred went back to same sexual preferences as before - People discover their sexual preferences; they don’t choose them - Sexual Preference develops early in childhood and usually doesn’t change - Perinatal castration in male rats = grow up with tendencies towards male rats - Prenatal testosterone exposure in females = preference in female partner rats - Indications that perinatal hormones do influence sexual orientation in humans (evidence sparse) o Ehrhardt (1985) interviewed adult women whose mothers had been exposed to stilbestrol (synthetic estrogen) during pregnancy.  Significantly more sexually attracted to women than control group  Therefore perinatal estrogen exposure does encourage homosexuality and bisexuality in women but its effect is relatively weak - Fraternal Birth Order Effect : the finding that the probability of a man’s being homosexual increases as a function of the number of older brothers he has. o Probability of a males being homosexual increases by 33% for every older brother he has and an estimated 15% og gay men can attribute homosexuality to Fraternal birth order effect. - Maternal Immune Hypothesis: proposed to explain fraternal birth order effect ; this hypothesis is that some mothers become progressively more immune to masculinizing hormones in male fetus and mothers immune system may deactivate maculating hormones in younger sons What triggers the Development of Sexual Attraction - In western countries most girls and boys experience attraction at age 10 (strange considering puberty at 10.5 to 11.5 years of agge) o May be due to adrenal cortex steroids which mature around the age of 10. (unlike gonadal maturation at 10.5 to 11.5) Is There a Difference in the Brain of Homosexuals and Heterosexuals - No reliable difference has been discovered yet!! Sexual Identity - Usually sexual identity coincides with a person’s anatomical sex, but not always - Transsexualism: a condition of sexual identity in which an individual believes that he or she is trapped in a bodu of the other sex. o Many seek surgical sexual reassignment o It is a very emotional devastating situation - Female to Male Procedure o More complex because penis has to be created and is therefore less satisfactory - Male to Female Procedure o Three times more prevalent o Must have in depth counseling before the process o Estrogen administration initiated to feminize the body (lifelong) o Penis and Testes surgically removed o Female genitalia constructed – vagina lined with skin and nerves from former penis (will have sensory nerve endings and therefore respond to sexual stimulus) o Some have cosmetic surgery to feminize face (Ex. remove adams apple) - One difficulty in determining Why transsexualism occurs is that there is no comparable syndrome in non humans Independence of Sexual Orientation and Sexual Identity - Someone with transsexualism can be attracted to males or females or both - Important to realize a particular sex related trait in an individual can lie at a midpoint between female and male norms - Challenges to mamawawa theory - Femaleness or Maleness depends on various attributes (body type, sexual orientation, and sexual identity) each of which can develop independently - Male and Female brains differ in many ways including: development at different timing and development of different mechanisms Chapter 14: Dreaming and Circadian Rhythms - Most will sleep around 175000 hours in their lifetime - Suggested amount of sleep: o Get as much as you can get (recommended 8 hours) o Or we sleep too much. If we sleep around 5 hours and therefore have more awake time The Case of the Woman Who Wouldn’t Sleep - Lady who would only sleep for an hour a day (body does it by itself)  without drowsiness - She sometimes wouldn’t sleep at all if has something interesting to do - In lab she went for two nights without sleep - Had electrodes attached to her and she promised she wouldn’t resist sleep - Finally she fell asleep for an hour and then woke up and was back to it Stages of Sleep - Many changes in human EEG in a night  although usually high voltage and slow there are period of the night that are associated with low voltage fast waves (similar to those when we are awake) - Rapid Eye Movement (REM) : occur under closed eyelids of sleepers during these periods of low voltage, fast EEG activity o Berger and Oswald discovered: loss of electromyographic activity in neck muscles during this time too - Three Standard Psychophysiological bases for defining stages of sleep: o Electroencephalogram (EEG) o Electrooculogram (EOG) o Electromyogram (EMG) Four Stages of Sleep EEG - Alpha waves : waxing and wanding bursts of 8- to 12-Hz EEG waves (happens when person closes their eyes and prepares for sleep). - Transition at Stage 1 sleep : low – voltage high frequency signal (similar to but slower than alert awakeness) - Gradual increase in EEG voltage and decrease in EEG frequency through progression from stage 1 to 2,3 and4 - In Stage 2: EEG is punctuated by : o K Complexes: single large negative wave (upward deflection) followed by single large positive wave(downward deflection) o Sleep Spindle: a 1- to 2- second waxing and waning burst of 12- to 14-Hz waves - Stage 3: defined by occasional presence of Delta Waves: the largest and slowest of the EEG waves - Stage 4: defined by predominance of Delta Waves o Stay at stage four for a while o And then drift back to stage 1 - Each cycle takes about 90 minutes o As the hours continue less and less time is spent in the later stages and longer time is spent in stage 1 - There are periods of time when the person is awake through the night even though person may not remember - Stage 1 = REM sleep Stage 2,3,4 = NREM - Stage 3 and 4 also called = slow –wave sleep (after delta waves) - Other physiological correlations with REM o Cerebral Activity = (oxygen consumption , blood flow, and neural firing) increases to waking levels in many brain structures o Increase in variability in the Autonomic nervous system (blood pressure, pulse, and respiration) o Muscle extremities may twitch o Penile erection can occur REM Sleep and Dreaming - Nathaniel Kleitman’s Laboratory (1953) o REM = dreaming?? emotionaly charged??  physiological  80% of REM sleep compared to 7% of NREM sleep led to dream recall  NREM dreams tended to take place in the sense of “I was falling”  While REM sleep tended to be more narrative stories Testing Common Beliefs About Dreaming - Following 5 beliefs about dreaming inspected o External stimuli being incorporated into a dream  Dement and Wolpert sprinkled water on patients while sleeping and then woke them up a few minutes later  In 14 of 33 cases water was incorporated o Some suggest dreams run on real time  Dement and Kleitman: let patient stay in REM for 5 or 15 minutes and then woke them and asked how long they thought they were dreaming, 92 out of 111 were correct o Some claim they don’t dream BUT they actually have as much REM sleep as normal dreamers  They do report dreams when awakened in REM but do so less often o Penile erection is NOT associated all the time with sexual dreams  Even babies have penile erections during their sleep o Sleepwalking (somnambulism) and sleep talking (somniloquy) are not associated with REM and can occur in any stage but often during transition to awakeness  Sleepwalking tends to occur in stage 3 and 4 of cycle and not when core is relaxed Interpretation of Dreams - Freud believed by unacceptable repressed wishes often of sexual nature o Our manifest dreams are merely disguised as our latent (real) dreams - Hobson’s (1989) theory : Activation Synthesis Theory o The information supplied supplied to the cortex during REM sleep is largely random and that the resulting dream is the cortex’s effort to make sense of these random signals o Based on observation that: many brain stem circuits become active and bombard cerebral cortex with neural signals (when in REM) Why Do we Slep and Why Do We Sleep When We Do? - Two theories of sleep have been proposed o Recuperation theories: being awake disrupts the homeostasis (internal physiological stability) of the body in some way and sleep is required to restore it  Function of sleep to restore energy levels  Sleepiness triggered by a deviation from homeostasis caused by wakefulness o Adaptation theories : sleep isn’t a reaction of disruptive effects of being awake but the result of an internal 24 hour timing system – therefore humans are programmed to sleep at night regardless of what we have done during the day  We have evolved to sleep at night because it protects us from accident and avoid predation  Focuses more on when we sleep rather than the function  Sleep like reproductive behavior, in the sense that we are highly motivated to engage in it, but we don’t need it to stay healthy o Some say that over evolution we got everything done that we needed during the day (food, eat….) and therefore sleeping at night was a way to conserve energy resources and be less susceptive to mishap Comparative Analysis of Sleep - Both mammals and birds sleep like humans do in similar patterns - Sleep in amphibians, insects, fish and reptiles are less clear : some display inactivity and unresponsiveness but hasn’t been comparative to the sleep of mammals - Four general comparable conclusions: o Mammals and birds sleep suggesting that it is a physiological function rather than protecting animals and conserving energy  Evidence is strongest in animals that are in increased risk of predation when sleeping (antelopes)  Some have evolved to allow for more protection when sleeping ; dolphins only sleep with half of their brain so the other half can keep them breathing o Mammals and birds sleeping suggest it is not just a high order human function o Large difference in sleep time between species suggests although sleep necessary for survival it is not needed in large quantities  Horses = 2 – 3 hours ; sloths = 20 hours  We have to take not that different settings may allow different sleep patterns. AKA in captivity may sleep more than in the wild o Why do some animals sleep for such a long period of time compared to others? Strong correlation found between animal body size, level of activity, body temperature and their sleep time.  The fact that sloths sleep 20 hours a day is a strong indicator that sleep is a compensatory response to energy expenditure  There has been theories that state sleep time is related to how at risk they are of predation when sleeping and how much time is needed for feeding itself and other survival tactics
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