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1 Chapter 13—Hormones and Sex MEN – ARE – MEN – AND – WOMEN – ARE – WOMEN ASSUMPTION 1. A.K.A. “Mamawawa” 2. Is seductive; seems so right that we’re continuously drawn to it w/o considering alternative views 3. Tendency to think about femaleness & maleness as discrete, mutually exclusive, opposite categories DEVELOPMENTAL AND ACTIVATIONAL EFFECTS OF SEX HORMONES 1. Hormones influences sex in 2 fundamentally different ways: a. By influencing the development from conception to sexual maturity of the anatomical, physiological, & behavioral characteristics that distinguish one as female or males b. By activating the reproduction-related behavior of sexually mature adults I.

Neuroendocrine System a. Endocrine Glands: Organs whose primary function appears to be the release of hormones b. Glands i. Exocrine Glands: Release their chemicals into ducts, which carry them to their targets, mostly on surface of body (e.g., Sweat Glands) ii. Endocrine Glands (Ductless Glands): Release their chemicals (hormones) directly into the circulatory system 1. Once released by endocrine gland, hormone travels via circulatory system until it reaches the target it normally exerts its effects iii. GONADS 1. Gonads: The male testes and the female ovaries 2. Copulation: Sexual intercourse 3. Sex Chromosomes: Contain the genetic programs that direct sexual development 4. Y-chromosome genes appear to encode only 66 proteins in comparison to 615 for the larger X-chromosome genes c. Hormones i. Vertebrate hormones fall into 1 of 3 classes: 1. Amino acid derivatives 2. Peptides & Proteins 3. Steroids ii. Amino Acid Derivatives: Hormones that are synthesized in a few simple steps from an amino acid molecule 1. Example: Epinephrine (Released from adrenal medulla & synthesized from tyrosine) iii. Peptide Hormones & Protein Hormones: Chains of amino acids—peptide hormones are short chains, & protein hormones are long chains iv. Steroid Hormones: Hormones that are synthesized from Cholesterol (A type of fat molecule) 1. Influence sexual development & activation of adult sexual behavior 2. Small & fat-soluble 3. Can readily penetrate cell membranes & often affect cells in a 2nd way 4. Once inside cell, steroid molecules can bind to receptors in the cytoplasm or nucleus & by so doing, directly influence gene expression (amino acid derivative hormones & peptide hormones affect gene expression less commonly & by less direct mechanisms) 5. Tend to have the most diverse & long-lasting effects on cellular function v. SEX STEROIDS 1. 2 main classes of gonadal hormones:

2 a. Androgens i. Most common is testosterone b. Estrogens i. Most common is estradiol 2. Progestins: 3rd class of steroid hormones a. Most common is progesterone i. In females, its function is to prepare the uterus & breasts for pregnancy ii. In males, its function is unclear, but may play role in sperm cell metabolism 3. Adrenal Cortex: The outer layer of the adrenal glands a. Primary function is the regulation of glucose & salt levels in the blood b. It releases small amounts of all the sex steroids released by the gonads d. The Pituitary i. Frequently referred to as the master gland bc most of its hormones are tropic hormones ii. Tropic Hormones: Primary function is to influence the release of hormones from other glands 1. Ex: Gonadotropin: Pituitary tropic hormone that travels through the circulatory system to the gonads, where it stimulates the release of gonadal hormones iii. Pituitary is really 2 glands 1. Posterior Pituitary: Develops from a small outgrowth of hypothalamic tissue that eventually comes to dangle from the hypothalamus on the end of the pituitary stalk 2. Anterior Pituitary: Begins as part of the same embryonic tissue that eventually develops into the roof of the mouth; during the course of development, it pinches off & migrates upward to assume its position next to the posterior pituitary a. Releases tropic hormones; thus, it is the anterior pituitary in particular, rather than the pituitary in general, that qualifies as the master gland iv. FEMALE GONADAL HORMONE LEVELS ARE CYCLIC; MALE GONADAL HORMONE LEVELS ARE STEADY. 1. Major diff b/w endocrine function of females & males is that in human females, the levels of gonadal & gonadotropic hormones go through a cycle that repeats itself every 28 days or so a. It is the more-or-less regular hormone fluctuations that control the female menstrual cycle 2. Hypothesis assuming that an inheritance difference b/w male & female anterior pituitary was basis for diff in male & female patterns of gonadotropic & gonadal hormone release a. Discounted by series of clever transplant studies conducted by Geoffrey Harris in 1950s i. IN studies, a cycling pituitary removed from a mature female rat became a steady-state pituitary when transplanted at the appropriate site in a male, & a steady-state pituitary removed from a mature male rat began to cycle once transplanted into a female ii. Established was that anterior pituitaries are not inherently female (cyclical) or male (steady-state); their patterns of hormone release are controlled by some other part of the body e. Control of the Pituitary i. Hypothalamic stimulation & lesion experiments quickly established that the hypothalamus is the regulator of the anterior pituitary

3 ii. Anterior pituitary does not receive any neural input whatsoever from the hypothalamus or from any other neural structure iii. CONTROL OF THE ANTERIOR AND POSTERIOR PITUITARY BY THE HYPOTHALAMUS 1. 2 diff mechanisms by which the hypothalamus controls the pituitary: a. 1 for the posterior pituitary b. 1 for the anterior pituitary 2. 2 major hormones of posterior pituitary a. Vasopressin & Oxytocin i. Peptide hormones that are synthesized in the cell bodies of neurons in the paraventricular nuclei & supraoptic nuclei on each side of the hypothalamus ii. Then transported along the axons of these neurons to their terminals in posterior pituitary & are stored there until the arrival of action potentials causes them to be released into the bloodstream iii. Neurosecretory Cells: Neurons that release hormones into general circulation 3. Oxytocin: Stimulates contractions of the uterus during labor & the ejection of milk during suckling 4. Vasopressin (A.K.A. Antidiuretic Hormone): Facilitates the reabsorption of water by the kidneys 5. Oxytocin & Vasopressin seem to influence stress-coping & social responses 6. Harris suggested that the release of hormones from the anterior pituitary was itself regulated by hormones released from the hypothalamus a. 2 findings provided early support for hypothesis: i. Hypothalamopituitary Portal System: The vascular network that carries hormones from the hypothalamus to the anterior pituitary ii. Discovery that cutting the portal veins of the pituitary stalk disrupts the release of anterior pituitary hormones until damaged veins regenerate b. Portal Vein: Vein that connects one capillary network w/ another f. Discovery of Hypothalamic Releasing Hormones i. Releasing Hormones: The hypothalamic hormones that were thought to stimulate the release of an anterior pituitary hormone ii. Release-Inhibiting Hormones: The hypothalamic hormones thought to inhibit the release of an anterior pituitary hormone iii. Thyrotropin-Releasing Hormone: Trigger the release of thyrotropin from the anterior pituitary, which in turn stimulates the release of hormones from the thyroid gland 1. Discovered by Schally & his colleagues a. Confirmed that hypothalamic releasing hormones control the release of hormones from the anterior pituitary & thus provided the major impetus for the isolation & synthesis of other releasing & release-inhibiting hormones iv. Gonadotropin-Releasing Hormone: Stimulates the release of both of the anterior pituitary’s gonadotropins: Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) g. Regulation of Hormone Levels i. REGULARION BY NEURAL SIGNALS 1. All endocrine glands, except the anterior pituitary, are regulated by signals from the nervous system

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2. Endocrine glands are located in the brain (i.e., the pituitary & pineal gland) are regulated by cerebral neurons 3. Those located outside the CNS are innervated by the ANS—usually by both the sympathetic and parasympathetic branches, often have opposite effects on hormone release 4. Effects of experience on hormone release are usually mediated by signals from nervous system 5. *Remember: Hormone release can be regulated by experience* ii. REGULATION BY HORMONAL SIGNALS 1. Hormones themselves also influence hormone release 2. Regulation of endocrine function by the anterior pituitary is not a one-way street 3. Circulating hormones can often provide feedback to the very structures that influence their release: pituitary gland, hypothalamus, & other sites in the brain 4. Function of most hormonal feedback is the maintenance of stable blood levels of the hormones a. High gonadal hormone levels usually have effects on hypothalamus & pituitary that decrease subsequent gonadal hormone release, & low levels usually have effects that increase hormone release iii. REGULATION BY NONHORMONAL CHEMICALS 1. Glucose, calcium, & sodium levels in blood all influence the release of particular hormones a. Ex: Increases in blood glucose increases release of insulin from pancreas; in turn insulin reduces blood glucose levels iv. PULSATILE HORMONE RELEASE 1. Hormones tend to be released in pulses a. Discharged several times per day in large surges, typically last no more than a few mins 2. Consequence is that there are often large min-to-min fluctuations in the levels of circulating hormones h. Summary Model of Gonadal Endocrine Regulation i. Brain controls the release of gonadotropin-releasing hormone from the hypothalamus into the hypothalamopituitary portal system, which carries it to the anterior pituitary ii. In anterior pituitary, the gonadotropin-releasing hormone stimulates the release of gonadotropins, which are carried by the circulatory system to the gonads iii. In response to gonadotropins, gonads release androgens, estrogens, & progestins, which feed back into the pituitary & hypothalamus to regulate subsequent gonadal hormone release Hormones and Sexual Development of the Body a. Dimorphic: Come in one of two models b. Sexual Differentiation i. Begins at fertilization w/ production of 1 of 2 diff kinds of zygotes 1. XX (female) pair of sex chromosomes 2. XY (male) pair of sex chromosomes ii. We are all genetically programmed to develop female bodies; genetic males develop male bodies only when their female program of development has been overruled iii. FETAL HORMONES AND DEVELOPMENT OF REPRODUCTIVE ORGANS 1. Primordial Gonads: Existing at the beginning a. Have an outer covering (Cortex) which has potential to develop into an ovary b. Has internal core (Medulla) which has potential to develop into a testis

5 2. Sry Gene: On the Y chromosome of males triggers the synthesis of Sry protein 3. Sry Protein: Causes the medulla of each primordial gonad to grow & to develop into a testis 4. Intersexed Persons: Male w/ ovaries, Female w/ testis iv. INTERNAL REPRODUCTIVE DUCTS 1. 6 weeks after fertilization, both males & females have 2 complete sets of reproductive ducts 2. Wolffian System: Has the capacity to develop into the male reproductive ducts (e.g., the seminal vesicles, vas deferens) 3. Seminal Vesicles: Hold the fluid in which sperms cells are ejaculated 4. Vas Deferens: Which the sperm travels to the seminal vesicles 5. Müllerian System: Has the capacity to develop into the female ducts (e.g., uterus, fallopian tubes) 6. 3rd month of fetal development, testes secrete testosterone & Müllerian-inhibiting substance a. Testosterone stimulates the development of the Wolffian system b. Müllerian-Inhibiting substance causes the Müllerian system to degenerate & the testes to descend into the scrotum 7. Bc testosterone that triggers Wolffian development, genetic females who are injected w/ testosterone during appropriate fetal period develop male reproductive ducts along w/ their female ones 8. Differentiation of internal ducts of female reproductive system isn’t under the control of ovarian hormones; ovaries are almost completely inactive during fetal development 9. Development of Müllerian system occurs in any fetus that isn’t exposed to testicular hormones during critical fetal period 10. Ovariectomy: Removal of the ovaries 11. Orchidectomy: Removal of the testes 12. Gonadectomy A.K.A. Castration: Surgical removal of gonads—either ovaries or testes v. EXTERNAL REPRODRUCTIVE ORGANS 1. Genitals: External reproductive organs 2. In both male & female genitals develop from same precursor, bipotential precursor 3. @ end of 2nd month of pregnancy, bipotential precursor of external reproductive organs consist of 4 parts: Glans, Urethral folds, Lateral bodies, & Labioscrotal swellings a. Glans  grows into head of penis (M) or clitoris (F) b. Urethral Folds  fuse (M) or enlarge to become labia minora (F) c. Lateral Bodies  form shaft of penis (M) or hood of clitoris (F) d. Labioscrotal Swellings  form scrotum (M) or labia majora (F) 4. Development of external genitals is controlled by presence or absence of testosterone c. Puberty: Hormones and Development of Secondary Sex Characteristics i. Puberty: The transitional period b/w childhood & adulthood during which fertilization is achieved, adolescent growth spurt occurs, & secondary sex characteristics develop 1. Associated w/ an increase in release of hormones by anterior pituitary ii. Secondary Sex Characteristics: Features other than the reproductive organs that distinguish sexually mature males & females

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iii. Growth Hormone: Only anterior pituitary hormone that doesn’t have a gland as its primary target iv. Increase in release of growth hormone acts directly on bone & muscle tissue to produce the pubertal growth spurt v. Increase in release of gonadotropic hormone & adrenocorticotropic hormone cause the gonads & adrenal cortex to increase their release of gonadal & adrenal hormones 1. In turn initiate the maturation of genitals & development of secondary sex characteristics vi. Pubertal males: 1. Androgen levels are higher than estrogen levels, masculinization is the result vii. Pubertal females: 1. Estrogens predominate & result is feminization viii. Individuals who are castrated b4 puberty don’t become sexually mature unless they receive replacement injections of androgens or estrogens ix. Androstenedione: Androgen released primarily by adrenal cortex, typically responsible for growth of pubic hair & axillary hair in females x. Male pattern is a pyramid, female pattern is an inverted pyramid Hormones and Sexual Development of Brain and Behavior a. Sex Differences in the Brain i. Male brains tend to be 15% larger than those of females 1. Diffs in ave vol of various cortical areas, nuclei, & fiber tracts, in # & types of neural & glial cells that compose various structures, in plasticity of certain brain structures, & in #s & types of synapses that connect the cells in various structures ii. FIRST DISCOVERY OF A SEX DIFFERENCE IN MAMMALIAN BRAIN FUNCTION 1. Focused on factors that control the development of steady & cyclic patterns of gonadotropin release in males & females 2. Seminal experiments were conducted by Pfeiffer in 1936 a. Some neonatal rats (M & F) were gonadectomized & some weren’t, & some received gonad transplants (ovaries or tests) & some didn’t b. Found that gonadectomizing neonatal rats of either genetic sex caused them to develop into adults w/ female cyclic pattern of gonadotropin release c. Transplantation of testes into gonadectomized or intact female neonatal rats caused them to develop into adults w/ steady male pattern of gonadotropin release d. Transplantation of ovaries had no effect on pattern of hormone release e. Concluded that female cyclic pattern of gonadotropin release develops unless the preprogrammed female cyclicity is overridden by testosterone during perinatal development f. Incorrectly concluded that presence or absence of testicular hormones in neonatal rats influenced the development of the pituitary bc he was not aware that the release gonadotropins from anterior pituitary is controlled by hypothalamus g. Once discovered, it became apparent that Pfeiffer’s experiments provided the 1st evidence of role of perinatal androgens in overrising he preprogrammed cyclic female pattern of gonadotropin release from hypothalamus & initiating the development of steady male pattern iii. AROMATIZATION HYPOTHESIS

7 1. Aromatization: The chemical process by which testosterone is converted to estradiol 2. Enzyme: Protein that influences a biochemical reaction w/o participating in it 3. Aromatization Hypothesis: Perinatal testosterone doesn’t directly masculinize the brain; brain is masculinized by estradiol that has been aromatized from perinatal testosterone 4. Evidence is of 2 types: a. Findings demonstrating masculinizing effects on the brain of early estradiol injections b. Findings showing masculinization of the brain doesn’t occur in response to testosterone administered w/ agents that block aromatization or in response to androgens that cannot be aromatized 5. Alpha Fetoprotein: Present in blood of rodents during perinatal period & it deactivates circulating estradiol by binding to it a. Its function in humans remains controversial b. Doesn’t readily penetrate the BBB iv. SEX DIFFERENCES IN THE BRAIN: THE MODERN PERSPECTIVE 1. Most of sex diffs in brain that have been documented are slight, variable, & statistical, but usually plenty of overlap 2. Sex diffs develop independently in diff parts of the brain @ diff points in time & by diff mechanisms a. Some aren’t manifested until puberty & those are unlikely to be product of perinatal hormones 3. 2 factors have proven to play little or no role in sexual differentiation of reproductive organs do play a role in sexual differentiation of the brain: a. Sex chromosomes have been found to influence brain development independent of their effect on hormones i. Ex: diff patterns of gene expression exist in brains of male & female mice even b4 gonads become functional b. Although female program of reproductive organ development proceeds typically in absence of gonadal steroids, recent evidence suggests that estradiol plays an active role i. Knockout mice w/o gene that forms estradiol receptors don’t display a typical female pattern of brain development 4. Female program of development is default program explains very well differentiation of reproductive organs & hypothalamus, it falters badly when it comes to differentiation of other parts of the brain 5. Complex mechanisms are diff in diff mammalian species a. Aromatization plays a less prominent role in primates than in rats & mice b. Development of Sex Differences in Behavior i. DEVELOPMENT OF REPRODUCTIVE BEHAVIORS IN LABORATORY ANIMALS 1. Phoenix & colleagues a. 1st to demonstrate that perinatal injection of testosterone masculinizes & defeminizes a genetic female’s adult reproductive behavior b. When adults’ females were injected w/ progesterone & estradiol & mounted by males displayed less lordosis 2. Lordosis: The intromission-facilitating arched-back posture that signals female rodent receptivity

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3. Lack of early exposure of male rats to testosterone feminizes & demasculinizes their reproductive behavior as adults 4. Male rats castrated shortly after birth failed to display typical male copulatory pattern of mounting, intromission, & ejaculation when as adults they were treated w/ testosterone & given access to a sexually receptive female, & when they were injected w/ estrogen & progesterone as adults, they exhibited more lordosis than uncastrated controls 5. Aromatization of perinatal testosterone to estradiol seems to be important for defeminization & masculinization of rodent copulatory behavior a. Aromatization doesn’t seem to be critical for these effect in monkeys 6. Timing is critical when it deals w/ the effects of perinatal testosterone on behavioral development 7. Proceptive Behaviors: Solicitation behaviors a. We know less about role of hormones in development of proceptive behaviors bc research has focused on copulatory a...