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Quiz 4 Study Guide

by: jjb13n

Quiz 4 Study Guide PSB 3004C

GPA 2.54

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Material for quiz 4
Physiological Psychology
Dr Hull
Study Guide
50 ?




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This 8 page Study Guide was uploaded by jjb13n on Thursday March 3, 2016. The Study Guide belongs to PSB 3004C at Florida State University taught by Dr Hull in Spring 2016. Since its upload, it has received 137 views. For similar materials see Physiological Psychology in Psychlogy at Florida State University.


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Date Created: 03/03/16
1. What is capacitation in sperm? What is the acrosome reaction? Why is it important?  Capacitation: Enzymes in the uterus/oviduct eat away the masking proteins.  (Sperm can live only a few hrs after capacitation.)   Acrosome reaction: Receptors exposed by capacitation bind to zona p., release  enzymes that eat through it.  Binding to ovum à Ca++ release in ovum à enzymes cause zona p. to become impenetrable by any more sperm. 2. What happens to the zona pellucida after a sperm penetrates the oocyte? 3. How long does it take the pronucleus in the oocyte to form after penetration by a  sperm?    About 4­6 hours after penetration.  4. What do the sperm and oocyte pronuclei do as soon as the oocyte pronucleus forms?  Male and female pronuclei replicate (do not combine into 1 nucleus);  replicated chromosomes line up in metaphase, separate into 2 daughter cells.  THEN male & female chromosomes combine into 1 nucleus/cell.   5. What is a blastocyst, and what does it do?  Blastocyst: A thin­walled hollow structure in early embryonic development  that contains a cluster of cells called the inner cell mass from which the  embryo arises.  32­cell blastocyst “hatches” from Z.P. & implants in endometrium:  beginning of pregnancy   6. By what age does the fetus begin to kick, suck its thumb, drink amniotic fluid,  urinate, wake & sleep?    After 14 – 16 wks: kicks, sucks thumb, drinks amniotic fluid, urinates,  wakes, sleeps (mostly REM). But brain very immature.   7. What is the main source of P after ~14 – 16 weeks post­conception?  Fetus takes control of mother: fetal side of placenta secretes P; fetal  adrenal à androgens, aromatized to E by placenta.   8. What is the DAX 1 gene?    The gene that encourages the developing fetus’ body to create ovaries.   9. What is gonadal intersexuality (true hermaphroditism)?  What are 2 ways it can be  produced?  Gonad with testicular tissue on the left and ovarian tissue on the right.   Can occur by early fusion of brother & sister embryos, by X inactivation  in XX fetus with SRY on one X, or 2 sperm (1X & 1Y) fertilizing an  ovum & 1 of its polar bodies. 10. What is X inactivation, and why is it important?  Without X inactivation, females would produce twice as much of these  proteins as males. 11. What is the origin and destination of migrating germ cells that will become sperm or  oocytes?  Germ cells that à oocytes and sperm arise from yolk sac, migrate to  genital ridge 12. What are Müllerian ducts?  What do they need to develop? 13. What are Wolffian  ducts?  What do they need to develop?  Males: antimüllerian hormone (AMH, a.k.a. Müllerian Inhibiting  Hormone, MIH) à Mullerian ducts go away; T à Wolffian duct  Females: No MIHà Müllerian ducts stay; no Tà no Wolffian ducts (Photo for questions 12 and 13) 14. What is Turner syndrome?  What are some symptoms?  Turner syndrome (XO) individuals are phenotypic females who do not enter  puberty and are infertile o XO genotype o Ovaries not fully developed à no steroid hormones o Must be treated with hormones to induce puberty. o Poor visuospatial skills o Most women with Turner’s syndrome lack normal ovaries. o Germ cells in the ovary require 2 X chromosomes to live. o They have short stature, broad chests, and webbed necks. o However, some have been quite successful. 15. What is Klinefelter syndrome?  What are some symptoms?  Klinefelter syndrome (XXY) individuals are phenotypic males who are generally  tall with somewhat feminized secondary sex characteristics and low testosterone  levels  Klinefelter syndrome: XXY, XXXY  Male, tall, small testes, breast development, sparse facial hair, low T, infertile (2   DAX­1 genes, poor language skills. 16. How can syndromes like XO, XXY, or XYY occur? 17. Describe androgen insensitivity syndrome: its cause and symptoms.  XY  Mutation of gene for androgen  receptor  (on X chromosome)  Insensitive to T  Normal testesà AMH & T  Woffian fail: no T­receptor  Mullerian ducts inhibited by AMH  Complete/partial 18. Describe congenital adrenal hyperplasia (CAH): its cause and symptoms in males and females.  Prenatal exposure to androgens: o Exposure to artificial steroid hormones (e.g., diethylstilbestrol,  medroxyprogesterone , etc.) can masculinize reproductive function and  behavior o Congenital adrenal hyperplasia (CAH):   Defect in enzyme that à cortisol  Low Cort à high ACTH from anterior pituitary:  “tries” to get  adrenal glands to produce more cortisol  Adrenals increase what they can produce: androgens and some  other steroids. o In male: differentiation OK, but early puberty and cessation of growth. o In female: enlarged clitoris and fused labia. o Play more with boys’ toys, less interested in motherhood, more inclined to male­typical activities and careers, more likely to be attracted to women,  but more hetero­ than lesbian, excel in visuospatial tasks 19. Describe 5­alpha reductase deficiency: its cause and symptoms.  Normal internal genitalia: testes secrete T, AMH (a.k.a. MIH) causes Mullerian  ducts to degenerate.  Lack of DHT leads to inadequate masculinization of external genitalia at birth  (DHT more potent than T)  Testes in labia or inguinal canal  Urogenital sinus: urethra & blind vagina  Prostate gland: small or absent  At puberty, lots of T à testes descend, scrotum darkens, phallus enlarges,  muscular, deep voice.  Transition to being male is easier because   Male role is valued in their society.  They did have T perinatally to masculinize their brain. 20. What is INAH­3, and why are people interested in it? Third interstitial nucleus of the anterior hypothalamus (INAH3) INAH3 is larger in men than in women, and larger in straight than in gay men. However, there is considerable overlap in size among females, males & gay men  LeVay reported that INAH 3 was also smaller in gay men than in straight men.  This is probably not just because gay men had brain degeneration due to AIDS.  There was at least 1 gay man who died of a heart attack, not AIDS, and his INAH 3 was also smaller than in straight men.  The other 3 INAH nuclei were NOT smaller in gay men.  Therefore, not  just a general degeneration.  However, we don’t know for sure what INAH 3 does  21. Describe the sex differences in SDN­POA and AVPV of rats.  What causes the  differences?  Sexually dimorphic nucleus (SDN) is larger in male rats than in females.   (Homologous to INAH3) o Same size in male and female fetuses before day 18 of gestation o T surges in males (day 18 of gestation and again ~ birth) à larger SDN in  males > females o Neurons die in females due to lack of T during early development; can’t  be “rescued” by T injections after 1 week postnatal. o T à E directly in MPOA is necessary. o Castration in adulthood à no effect o Female rats have larger AVPV (anteroventral periventricular nucleus) than do males. o Perinatal T decreases AVPV size – the opposite of its effect on SDN­POA o AVPV is involved in the positive feedback of E à LH surge. 22. Describe the effects of maternal stress on sex differentiation of rats.  Ingeborg Ward confined pregnant female rats under bright lights for 20 min x 3  times per day.  Male offspring were demasculinized in adulthood.  Stress à prenatal T surge occurred 2 days too early—before neurons were born in  the SDN­POA.  Therefore, the T surge fell on “deaf ears.”  Similar effects were found when mother rat received alcohol, cannabinol, or a  dopamine antagonist. 23. Describe 3 nonsexual sex differences.  Girls: wider hips; boys: wider shoulders  By adulthood, men have 50% more bone and muscle mass.  Women have higher  body fat %.  These are averages — there is great individual variability. 24. What are 3 factors that may influence the timing of pubertal development?  Puberty is starting at an earlier age o Nutrition o Environmental pollutants o Genetic changes 25. What are leptin and kisspeptin?  Leptin: hormone from fat cells  Mutation of leptin gene à no puberty  Leptin à kisspeptin (from several hypothalamic nuclei) à GnRH neurons  (MPOA)  Lack of kisspeptin receptor à no puberty  Kisspeptin  a protein molecule that is responsible for triggering the onset of puberty in humans. C21: after the KiSS­1 gene that produces it.


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