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Department
Psychology
Course
PSB 2000
Professor
Berkley
Semester
Fall

Description
Organizing and Activating Effects of Hormones o •Know the 3 classes of sex steroid hormones and their synthesis pathway. Know examples of each class (ie, testosterone is an androgen). o 3 Classes of sex steroid hormones  Androgens: testosterone, DHT  Estrogens: Estradiol  Progestins: progesterone o •Know the differences between organizational and activational effects of hormones. What are some examples of each type of effect in men and in women? o Organizing:  Occur mostly during sensitive periods in development (well before birth in humans)  Effects are generally permanent  Determine whether brain and body will develop male or female characteristics o Activating:  Occur any time in life, when a hormone temporarily activates a response  Effects last as long as hormone is present…thus generally temporary  Includes menstrual cycle in women, sexual excitement in men (and in women…there are some data…) o •What is the chromosomal difference between males and females? What is the region of the Y chromosome that is important for male development, and how/why does that trigger male development? What does it mean that “the default development pattern is female”? male XY female XX o SRY= sex determining region of Y chromosome o SRYmale development o No SRY female development o An individual’s sex is determined by the presence or absence of the Y chromosome. (default is female, presence of SRY gene signals male development factor) o Specifically, the SRY gene tells the gonads to develop into testes. o The testes release testosterone, and male development relies heavily on the presence of this testosterone as well as one of its metabolites, DHT. o So an individual’s sexual development could be altered by manipulating testosterone levels… o •How can a male be feminized/demasculinized or a female masculinized? o The “default” development pattern is female o w/o androgens or the ability to respond to androgens (androgen receptors), the individual develops as a female o SO, things that block androgen activity during a critical period of development can be feminizing/ demasculinizing in a genetic male  castration  lack of androgen receptors  drugs that block effects of testosterone (including marijuana, alcohol, haloperidol & cocaine) o To a much lesser extent, estrogens (including environmental estrogens) can alter the male pattern of development.  prostate gland (which stores sperm & releases it during intercourse) is especially vulnerable. o The critical period for organizing effects of hormones in rats is right around birth. o Testosterone at this time will masculinize genetic females in terms of behavior*, anatomy, and neuroanatomy o *If given T again again as adult, she will mount a receptive female (more later) o Males have larger sexually dimorphic nucleus (image to left) o Also, female hypothalamus generates cyclic pattern of hormone release (causing menstrual cycle). Male hypothalamus & masculinized female hypothalamus doesn’t o •Understand how hormones affect sexual behavior and know some evidence for those effects in rats and in humans. o Alter activity in certain brain regions  change the way the brain responds to certain stimuli. A few examples:  T and probably E decrease pain and anxiety  Decreases in T & E associated w/ memory problems  E stimulates growth of dendritic spines in hippocampus  E increases production of dopamine & serotonin receptors in nucleus accumbens, PFC, olfactory cortex, other cortical regions o •In terms of sexual behavior, hormones change activity in some brain regions & change sensitivity of penis, vagina and cervix. o •In what pattern do testosterone levels change in males? Do they also fluctuate in females? If so, in what pattern? o Sexual excitement highest when T is highest (15-25 yr old)  Higher T levels  more “partner-seeking” even if married  Decrease T  decrease sexual activity  Decrease T to control sex offenders  But T (alone) doesn’t cause these behaviors!  Sex offenders have average T levels, except child molesters whose T levels are especially high  Oxytocin also important in sexual behavior o •Fun fact: Viagra works by prolonging effects of nitric oxide (NO)  T increases release of NO  NO facilitates hypothalamus neurons important for sexual behavior & increases blood flow to penis o •What hormones are involved in the menstrual cycle? What are hormone levels (low, medium, high) when a woman is periovulatory? You do not need to know any details of the menstrual cycle beyond these questions. However, if is always good to have such knowledge of how the body functions! What changes in behavior do we see during the periovulatory phase? o Hypothalamus + pituitary + ovaries = menstrual cycle (more in Inquiring Minds slides)  Depends on 4 hormones: luteinizing hormone (LH), follicle- stimulating hormone (FSH), estrogen, progesterone o Certain changes when periovulatory  Periovulatory means that E is high, P is beginning to rise, T is as high as it gets in females; this is the few days surrounding ovulation.  More likely to initiate sexual behavior  Find erotica more pleasant and arousing  Prefer more masculine looking men and men who seem “athletic, competitive, and assertive, and who did not describe self as having a nice personality” for “short-term sexual relationship”  Lap dancers earn most tips (b/c feel/act sexier?) o •What are some examples of differences in the hypothalamus between males and females? o The critical period for organizing effects of hormones in rats is right around birth. o Testosterone at this time will masculinize genetic females in terms of behavior*, anatomy, and neuroanatomy o *If given T again again as adult, she will mount a receptive female (more later) o Males have larger sexually dimorphic nucleus (image to left) o Also, female hypothalamus generates cyclic pattern of hormone release (causing menstrual cycle). Male hypothalamus & masculinized female hypothalamus doesn’t o •What events stimulate oxytocin release and what behaviors are associated w/ oxytocin? o Released from posterior pituitary o Stimulates uterine contractions during & after delivery of baby o Stimulates mammary glands to release milk o Released by sexual pleasure, especially orgasm o Decreased anxiety after orgasm due to oxytocin  Could also be the source of reported anxiolitic effect of nursing o Important in pair bonds b/t mating partners o Important in pair bonds b/t mother and infant o •Parental behavior: what is some evidence that vasopressin is important in paternal behavior? In general, how do hormones prepare the female for motherhood? o E, prolactin (milk production, gathering wandering young), oxytocin prime mother before birth o Hormone receptors also change their expression pattern during pregnancy to prepare for motherhood  Increase in areas important for maternal behavior; decrease in areas important for sexual behavior…go figure! o In moms, experience is important too, and eventually parental behavior is accomplished by experience w/o the need for additional hormones (this is in rodents; in humans, hormone priming isn’t even needed) o Vasopressin (VP) important in paternal behavior  Male prairie voles have high VP levels & pair bond w/ female & help rear young (so considered “monogamous”)  Male meadow voles have low VP levels, & ignore female after mating (so considered “promiscuous”)  unless you genetically engineer them to make more VP, in which case they become monogamous! Variations in Sexual Behavior o •What are some differences in sexual behavior between males and females, and with a given sex? o b/t males and females  Number of partners  What is sought in a mate  Psychological components: jealousy o w/in sexes  Heterosexual, bisexual, homosexual o •Understand the difference between a person’s “gender” and their “sex”. Understand the difference between gender identity and sexual orientation. What does it mean that these are “continuous rather than categorical)? o Sex refers to genes (XX or XY); gender refers to with whom we identify and what we call ourselves, it is uniquely human o Sexual terminology  Gender versus sex  Gender identity versus sexual orientation  Gender identity: what you identify self as :male female  Sexual orientation: homo/heterosexual  Categorical versus continuous  Sexual orientation is more continuous for females; more categorical for males  Men seem to be more categorical in their sexual orientation; they are more likely to be either heterosexual or homosexual. Women, on the other hand, tend to be more flexible in their sexual orientation, less categorically heterosexual or homosexual.  o •What is evidence that genetics, hormones, prenatal hormone exposure, and/or prenatal stress have roles in sexual orientation? o Homosexuality strongly familial  Similarity in identical twins > than fraternal twins  Found for homosexual men and homosexual women o Genes cannot account for everything; influence of environment as well… epigenetics? o Why not select against such a gene?  Homosexual individuals help w/ child-rearing? Research says no.  The gene(s) is/are advantageous to female relatives or to heterosexual male relatives  Homosexual men’s moms & aunts had more kids on average, but not enough to compensate for his not having had any kids all  The gene(s) that cause homosexuality are recessive; trait only seen in homozygous condition; in heterozygous condition they confer reproductive advantage  Epigenetics! Experience adds chemical group to a certain gene  gene is inactivated  parent passes inactivated gene  heritable homosexuality w/o relying on the spread of a gene  Homosexual individual still pass on their genes… o Adult hormone levels do not differ o Prenatal hormone levels might have an effect  Animal studies sort of suggest this  Effects of castration on male rat pups or testosterone on female rate pups  Slight and partial feminizations in gay men and mascularaztions in lesbians begin before puberty o Bone length o Organizational effects of hormones affect brain development, and changes in these hormone levels can alter brain development. o Probability of homosexual orientation greater among men w/ older biological brothers  Mom’s immune system attacks some protein in other male fetuses?  Specific to right-handed, not left-handed younger brothers  but problems w/ these data? o Prenatal stress  Stress  increase endorphins  antagonize effects of T on hypothalamus  Stress  increase corticosterone  decrease T release  In animal models of maternal stress (maternal confinement & alcohol exposure)  Maternal confinement  As adults, male offspring more likely than offpsring of non-stressed moms to lordose in the presence of anther male; still engaged in male sexual behavior as well  Maternal confinement and alcohol  more losdosis & less male typical sexual behavior  In humans…In 2 out of 3 studies, moms of gay men reported more stress during pregnancy than moms of straight men o •What are some differences in brain anatomy between homosexual and heterosexual individuals? What about with regard to transgender individuals? o Hemisphere size:  R larger than L in heterosexual men; equal sizes in heterosexual women & homosexual men; homosexual females are intermediate o Amygdala:  L has more widespread connections than R in heterosexual females & homosexual males; vice versa in heterosexual males; homosexual females are intermediate o Anterior commissure:  gay men = straight women > straight men o SCN:  gay men > straight men (rats deprived of T during critical period have abnormal SCN & vary male/female preference thruout the day) o Third interstital nucleus of the anterior hypothalamus… o How do heterosexual and homosexual individuals differ in their response to pheromones? o Brain responds to pheromones differently:  Heterosexual women & homosexual men respond to AND (found in male sweat; activation in preoptic area & ventromedial hypothalamus)  Heterosexual men respond to EST (found in female urine; activation in paraventricular nuclei and dorsomedial nuclei of hypothalamus)  Lesbians respond to EST in a way that is partially similar to heterosexual males; also processed AND with main olfactory system rather than anterior hypothalamus.  “…coupling between hypothalamic neuronal circuits and sexual preferences.”  Transexuality  BNST is larger in men than women  No difference b/t heterosexual and homosexual men.  Small in male to female transexuals (more similar to women)  Large in female to male transexuals (more similar to men)  Therefore, the correlation is to sexual identity; not sexual orientation  In transexual men, BNST (forebrain region) is small, like in women; there is no difference b/t heterosexual and homosexual men. o •What is the relevance of data such as differences in bone length between gay and straight individuals? o Bone length in arms, legs, and hands  Longer in men than women; homosexual males shifted in female direction; homosexual females shifted in male direction o Bones in arms, legs and hands longer in straight vs. gay men & gay vs. straight women o What are pseudohermaphrodites or intersexes? o Intersexes: individuals whose sexual development is intermediate or ambiguous  incidence??  1 in 100 children born with some degree of sexual ambiguity  1 in 2000: ambiguity is large enough to make gender assignment difficult  what do you do??  several decades ago: surgically feminize the genitalia & raise as a female  now: identify on basis of external genitalia and raise as consistently as possible o •Know/understand Turner’s syndrome, Klinefelter’s syndrome, congential adrenal hyperplasia, androgen insensitivity syndrome, and DHT deficiency. o Turner’s S.  X0 genotype  Poor ovaries  Low hormone  Immature sex  Infertile  Female gender, heterosex.  98% spontaneously abort (10% of miscarriages) o Klinefelter’s S.  XXY genotype (but some cells XY)  SRY = male  Internal sex OK  Small testes  Low T  Low sperm  Gynecomastia  Male gender, heterosexual o Congenital Adrenal Hyperplasia (CAH)  Autosomal recessive  Too much testosterone during development  Normally, ACTH from pituitary  cortisol from adrenals  negative feedback of cortisol to pit to stop release of ACTH  CAH: limited ability to make cortisol  no feedback  lots of ACTH  adrenals release more of all hormones, including T  Okay if XY, but if XX:  presence of DHT (made from T) partially masculinizes the genitalia (& brain?)  ambiguous external genitalia (internal organs less affected); usually diagnosed at birth  sometimes surgical intervention at that time  individual is treated with cortisol to reduce high concentrations of CRH and ACTH  Childhood behavior: intermediate b/t boy and girl (figure 11.10)  Adult behavior: (compared to other women) fewer than ave. sexual encounters and fantasies, more physical aggression, less interest in infants, more interest in male- dominated occupations  gender is female  sexual orientation is mixed, but trends toward heterosexual  Minority of people w/ CAH are intersex…other problems include delayed or precocious puberty o Androgen insensitivity syndrome  genetic male (XY), female gender identity, heterosexual  mutation on X chromosome in the region encoding the androgen receptor; thus unresponsive to T, DHT  in utero:  SRY gene  TDF produces testes (undescended)  antimullerian hormone (testes) causes degeneration of Mullerian ducts thus, no internal reproductive organs develop  lack of DHT action feminizes external genitalia  at birth (if complete AIS):  baby appears to be female  child is raised as a girl (will have female gender identity and be heterosexual)  If incomplete but predominantly male, raised as boy  at puberty:  breasts enlarge, hips broaden, no menstrual cycle (b/c no ovaries), also little pubic hair (depends on androgens in both women and men)  lack of menstruation prompts physical exam  intervention at this time?  internal testes are removed  vaginal canal is lengthened o DHT Deficiency  occurs in the genetic male (XY)  fairly common in one isolated community in the Dominican Republic  a genetic mutation causing a defect in the enzyme 5a-reductase  results in low levels of DHT; normal T  In utero  Y chromosome (SRY gene)  testes develop but do not descend  normal levels of T: development of the Wollfian ducts; regression of Mullerian ducts  no DHT: feminization of external genitalia  •At birth & adolescence  baby appears female; child is raised as a girl  gender identity = female, but behavior is “tomboyish”  At puberty  very high levels of T act to partially masculinize the genitalia  gender identity is usually reassigned o •What is the current advise given to parents with a baby whose sex is intermediate? o Be honest and do nothing w/o informed consent o Identify as male or female based on predominant external genitalia o Rear child as consistently as possible, but be aware that the person will later be oriented toward males, females, both or neither o Do not perform surgery until the person is old enough to be involved in this decision. Circadian Rhythms and Sleep o What is a circadian rhythm? What are some of the physiological states that are determined by them? o Circadian rhythms are about a day in length. They match up nicely with the Earth’s night-day cycle when we’re exposed to sunlight on a daily basis. o however, if you remove these light/dark cues, the body still has circadian rhythms. o However, there is a slight offset: in the absence of light, the average person has a circadian duration of about 24 hours 11 minutes, so in the absence of external cues, a person will wake up and go to bed 11 minutes later each day, offsetting their schedule by an entire day every 130 days or so. o What varies over the course of the day?  Body temperature  Hormone levels  Sensitivity to drugs  Eating & drinking  Digestive & excretion  Etc. o How does light affect circadian rhythms? What hypothalamic nucleus is responsible for this? o Circadian rhythms are entrained by light. o Light activates a special group of photoreceptors in the retina.  These respond much more slowly to light.  They respond to long periods of light but not brief bursts. o The specialized ganglion cells project to the suprachiasmatic nucleus (SCN). o The SCN is in the hypothalamus. o It is mostly responsible for maintaining circadian rhythms. o What circadian hormone is released by the pineal gland? When is it highest/lowest? o The SCN indirectly projects to the pineal gland. o This inhibits the hormone, melatonin.  Under low light, melatonin production is disinhibited.  This makes melatonin levels increase/HIGH.  This makes us sleepy at night. o What happens when you implant SCN tissue from a normal hamster into the brain of a mutant hamster with a 20-hour rhythm? o Thus, it appears that the SCN is the brain’s circadian clock.  By altering the SCN experimentally, we can alter the brain’s circadian clock. o Destroying the SCN removes the circadian rhythm.  Hamsters with a destroyed SCN no longer experience circadian rhythms.  But you can restore the rhythm with transplanted brain tissue! o Take a normal hamster and remove its SCN.  Circad
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