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Unit 2 Lecture notes

by: Maureen Gaffney

Unit 2 Lecture notes PSY 209

Maureen Gaffney

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These notes cover all of Unit 2 and information that could be tested on the next exam.
Brain and Behavior
L. Yan
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Popular in Psychlogy

This 19 page Bundle was uploaded by Maureen Gaffney on Tuesday March 1, 2016. The Bundle belongs to PSY 209 at Michigan State University taught by L. Yan in Spring 2016. Since its upload, it has received 48 views. For similar materials see Brain and Behavior in Psychlogy at Michigan State University.


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Date Created: 03/01/16
Hormones 02/10/2016 ▯ Forms of chemical communications  Synaptic or neurocrine function—involves chemical release and diffusion across a synapse  Endocrine—a chemical is released into the bloodstream to act on target tissue ▯ Hormones  Chemical agents being produced in our body  Secreted by glands or endocrine cells—cells are in the glands  Travel through the blood  Act on target cells, such as neurons, with specialized receptors ▯ Where are hormones produced?  Brain—specifically the hypothalamus  Pituitary  Thyroid  Adrenal Gland  Pancreas  Gonads  Ovaries  Testes ▯ Types of Hormones  Protein/Peptide—water soluble  Amine—water soluble  Steroid—lipid(fat) soluble o Sex hormones ▯ Hormone  Protein and Amine o Bind to membrane receptors, 2 ndmessengers  Steroid o Nucleus receptor, act as transcription factor ▯ Transmitters vs. Hormones  Precise(Neurotransmiter) vs. Broad destination(hormones)  Rapid transient vs. slower/persistent effects o Exception: Adrenalin  All or none swith vs. intensity/probability of behavior o Digital vs. analog  Range of effects ▯ Hypothalamus and Pituitary  Neuroendocrine Cells in Hypothalamus o Fluoro-gold tracing o GnRh/GnIH  Gonadotrophin realizing hormone/POA, inhibiting hormone/PVN o GHRH/GHIH  Growth hormone releasing.inhibiting hormone  Sp,atrpcrinin/Arc o Prolactin-releasing peptide/Prolaction-inhibiting peptide o CRH  Corticotrpophin releasing hormone, PVN o TRH  Thyrotrophin-releasing hormone, mPVN o AVP/Oxytocin ▯ Pituitary  1cm^3, 1 g  Anterior pituitary(front)  Posterior pituitary(back)—vasopressin and Oxytocin o Network of capillaries ▯ Oxytocin and milk  A neuroendocrine reflex  Also: o Helps with the birth process o Promotes maternal care o Promote pair bonding  Mother-infant  Male-female  KO mice (when absent do not recognize the females he encountered)  Infusion Vasopressin  Antidiuretic Hormone(ADH) o Inhibit urine formation o Vessel contraction  Social behavior o Vasopressin and monogamy? ▯ Anteriro pituitary  FSH/LH  GH  Prolactin  TSH  ACTH (adrenocorticotropic hormone) ▯ Endocrine System  Adrenal Glands o Cortex/medulla o Cortex(outer layer)  Glucocotricoids  Mineralocorticoids  Sex hormones o Medulla (inside)  Epinephrine  Norepinephrine ▯ Endocrine regulation: negative feedback  CRH—ACTH—adrenal steroids  Adrenal steroids inhibit ACH and CRH production  Adrenal Steroids are produced by the cortex ▯ The gonads  Secrete the hormones  Produce the gametesw ▯ What is evolution?  The process by which a population of interbreeding individuals changes over long periods of time leading to diverse forms of life  One species can change into another o Species are not fixed o Changes are random o Like a tree, most branches fall off  How do they change: o The variation exists o Natural selection ▯ Darwin’s two great and separate accomplishments  Establishing the fact of evolution  Proposing a theory—natural selection ▯ Natural Selection  Four facts o Individuals are not identical o Some variations among individuals is inherited o Reproduction will increase population rapidly unles factors limit it o Not all the offspring survive  Variations among individuals affect the survival and reproduction ▯ Evidence  Domestication o Ex. Dogs  Homology o Common ancestor  Darwin’s Finches  Fossils ▯ Sexual Selection  Inter and intra-sexual selection ▯ Why care about evolution  In general o Where we come from, where we going o What makes us human  As neuroscientist o Variation: brain feature—behavior o Adaptation: environment—behavior—brain ▯ Unique brain feature correlates with unique behavior ▯ Similarities between Human and Rat Brains  All vertebrates have the same major subdivisions  Main differences are the absolute and relative size of those regions ▯ Neurons  Same kind of neuron in different species o Have different structures—bigger brain bigger neuron because need to connect more ▯ Absolute brain size  Absolute Size: number of neurons should support complexity of computation o False counterexamples Relative brain size  Relative to body size—allometry  Deviations from predicted size corresponds to relative cognitive ability o Large difference between lower and higher vertebrates o Variation within high vertebrates ▯ Factors contributing to large brains  Social brain hypothesis o Primates have complex social groups o Correlation between brain complexity and social behavior o Specialized brain structures  Foraging hypothesis o Fruit eating leads to larger brains than leave or insects Benefits of larger brain  More computational power o Innovation o Tool use o Social learning  More adaptation o Survive and cop with new environment  More attractive o Sexual selection ▯ Cost of larger brain  Long gestation period  Long infancy, childhoods  More energy o 2% weight, 20% energy  More gene ▯ ▯ Sample Exam Questions: ▯ 1. Steroid hormones are derived from  cholestrol ▯ 2. Steroid hormones typically exert their effects by  binding to intracellular receptors ▯ 3. Which of the following is not secreted by the pituitary?  Proestrogene ▯ 4. Male mice with knockouts of the BLANK gene display “social Amnesia,” failing to recognize previously ….  Oxytocin ▯ 5. The hormone that controls the milk letdown reflex is  oxytocin ▯ Brain Development ▯ The adult brain  3 pounds  200 types of neurons  100 billion of them ▯ ▯ Where does it begin ▯ Stem cells------- Neural Plate ▯ ▯ Neural plate—3 layers  Outer layer—ectoderm  Middle layer—mesoderm  Inner layer—endoderm ▯ 6 Stages of Nervous System Development ▯ 1. Neurogenesis—mitosis produces neurons ▯ 2. Cell Migration—cells move to establish distinct populations ▯ 3. Differentiation—cells become distinctive neurons or glial cells ▯ 4. Process Outgrowth and Synaptogenesis—establishment of synaptic connections ▯ 5. Neural Cell Death—selective death of some nerve cells ▯ 6. Synapse Rearrangement—loss or development of synapses, fine- tuning ▯ ▯ 1. Neurogenesis  The production of nerve cells o Nerve cells do not divide, progenitor cells line the inner surface of the neural tube o Mitosis occurs in the ventricular zone o Cells leave the ventricular zone and become either neurons or glial cells or back to progenitor cells  When are the Neurons born? o To find answer  A nucleic acid tagged with a label injected at a specific stage of life  Later, when you see labeled cells, you know when they were born ▯ 2. Migration  Move away from inner layer o Guided by radial glial cells o Along a glial scaffold o Some go parallel to surface, “hitching a ride”… ▯ 3. Differentiation  Neurons differ with respect to: o Shape, size o Transmitter they release o Receptors they have o And more  How does it happen o Cell-autonomous—variation in gene expression o Neural environment—by neighboring cells  Autonomous—cells fate is predetermined  Induction: is the influence of one set of cells on the fate by nearby cells ▯ 4. Process Outgrowth and Synaptogenesis  Process Outgrowth—the growth of axons and dendrites  Synaptogenesis—formation of synapses  Growth cones responding to signaling factors: o Chemoattractants—pulls targeting cells axon terminal closer? o Chemorepellents  Synaptogenesis o Chemoaffinity hypothesis—frog experiment—optic nerve if cut the frog neurons will reconnect o After injury the brain will try to reestablish the original connections  Reconnect the same fashion as before  Reconnect randomly, brains learns to interpret the signal o To determine which one frog experiment—eyeball put in backwards—opposite signal given  If frog sees fly above the tongue goes down, if frog sees fly below, flips tongue up  The connect signal in same fashion as before o Possible mechanism for chemoaffinirty  Gradient ▯ 5. Neuronal Cell death  In human brain neurogenesis produces 200 billion, half die  Apoptosis (cell death) normal part of development  Death genes( in each cell)—expressed only during apoptosis  Caspases—a family of proteases that cut up proteins and DNA  If cells don’t die then the brain will be double the size and won’t be able to survive  What determines which cells stay and which die? o Regulated by the connections they make—neurotrophic factors produced by target cells—  if they receive more neurotrophic factors more likely to survive ▯ 6. Synapse Refinement  motor neurons change their muscle unit connections with development  become more efficient  Synapses are eliminated over time o Peaks around 1 year and stabilizes around year 10  Synapse reaarangment (synaptic remodeling)—refines synaptic connections  One influence on synaptic survival is neural activity o A neurotrophic factor may contribute  What determines which synapses stay or go? o Neurotrophic factors o Axons compete at synaptic sites for trophic factors o The process fine tunes the synaptic connections  Hebbian synapses o Synapses that grow stronger or weaker depending on their effectiveness to driving their target cell o ▯ Stuff to know for test 2 ▯ Ventricular Layer is where nervous cells generate from ▯ Migrating neurons controlled by obliogcytes? Idk how to spell it ▯ Two mechanisms regulating neuronal differentiation included cell signaling and induction ▯ Axonal outgrowth is guided by chemoattractant and chemorepellent ▯ ▯ Sex hormones ▯ Hypothalamus—  Gonadotropin releasing hormone  Gonadotopin-inhibiting hormone o Males  FSH (Follicle stimulating hormone) stimulate the production of sperm  Most in adults 1.5-12.4 mlU/ml  Puberty: 0.3-10.0 mlU/ml  Before puberty:0-5.0 mlU/ml  LH (luteinizing hormone) stimulates production of Testosterone o Females  FSH stimulates the production of egg and Estadiol  Before Puberty: 0-4.0mlU/ml  During Puberty: 0.3-10.0 mlU/ml  Menstruating: 4.7-21.5 mlU/ml  Postmenopausal: 25.8-134.8 mlU/ml  Why do postmenopausal women have such high range? o Limited estrogen production and there is no negative feedback—no inhibition  LH stimulates production of testosterone—concerted into Estradiol—estrogen and progesterone?  LH surge: ovulations ▯ Castration: removal of testes  Chicken experiment—small, not aggressive, don’t mount hens, weak —without testes—deprived throughout development  Hamster experiment— o sex drive decreases after castration o testosterone therapy—sex drive goes back up  higher dose of testosterone didn’t do more than the low dose ▯ Organizational vs. Activational effects of Steroid hormones  Organization—permanent, occur during critical period in development—wire the brain  Activation—transient, commonly occur in adulthood, turn on behavior  Both types effect critical display of reproductive behaviors ▯ ▯ Sexual Behavior—Goal is to reproduce ▯ Types of Fertilization  External  Internal ▯ Four Stages of Sexual Behavior  Sexual Attraction  Appetitive behavior  Copulation  Postcopulatory behavior o Maternal and paternal care ▯ Human Sexual Behavior  Female conceal ovulation  Sex behavior around the cycle  Pair bonding—oxytocin released during sex?  Paternal involvement o Why do we develop into this sexual pattern?  Development of human brain—evolutionary perspective ▯ Coolidge effect  Refers to the faster resumption of mating behavior, with a different partner o Widespread—many species o Dopamine—related ▯ Experiment: Female rats ovulate or release eggs, every 4-5 days  If a female is willing to copulate, o sexually receptive or in estrus  high estrogen and progesterone near ovulation  Lordosis—receptivity allows intromissions o Back arching in female rats Neuron Circuitry Regulates Reproduction Behavior—KNOW THIS  Males o Medial preoptic Area(mPOA)—coordinates copulatory behavior o The mPOA project to the ventral midbrain then to the basal ganglia to coordinate mounting o Axons also project through the brainstem nuclei to the spinal cord—helps males reach ejaculation? o Males have larger mPOA then females and homosexual males  Females o The ventromedial hypothalamus (VMH) is crucial for lordosis o Estrogen increases dendritic trees of neurons in VMH o Estrogen also stimulates progesterone receptors in turn contribute to lordosis through increasing sensitivity to progesterone o Ventromedial hypothalamus—periaqueductal gray—medullary reticular formation—recticulospinal tract—spinal cord--lordosis ▯ Sex differentiation in brain and behavior  Verbal—girls develop earlier  Math  Reasoning o These differences are subtle  Androphilia vs. gynephilia—bigger difference ▯ Sex differences in Brain  mPOA larger in Males than females ▯ Cause of Sex differences in brain—hormonal difference in early development  Male have prenatal testosterone surges—around birth and then another surge at puberty  Female prenatal testosterone treatment o POA mascualinized o Behave like male  Female get testosterone injection at puberty—no effect Gender  First factor—Genetic Sex—chromosones  Gonad Sex—ovary or testes  Phenotypical sex—how we act. ▯ ▯ SRY—Sex determining region on Y chromosome  Will develop into testis—creates testosterone and AMH ▯ The primordial gonad expression of SRY testis (Know the functions of AMH and T)  AMH o Presence—regression of Mullerian Duct o Absence—Mullerian duct develop into fallopian tubes and uterus  Testosterone o Presence—Wolffian duct develop inot Vas Deference, seminal vesicle, prostate o Absence—regression of Wolffian duct  DHT (5 [alpha] reductase)—external sex organ presence—penis; absence—vagina ▯ Sex is determined early in life  Individual develops as a female without the SRY gene ▯ Gender Variations  Androgen insensitivity syndrome (AIS)—can secrete the hormones but body doesn’t respond to testosterone o XY o Respond to AMH, but not testosterone or DHT o Testes don’t descend but do secrete testosterone and AMH o No ovaries or uterus o Have a vagina o Same raised as boys, but most as girls  Congenital Adrenal hyperplasia (CAH) o Female exposure to androgens before birth o Intersex appearance o Glucocorticoid treatment prevent further androgen exposure surgery  5[Alpha] reductase deficiency o inherited disorder o Large families in Dominican Republic, Turkey and Egypt o Testosterone cannot be converted to DHT—a more active form  Internal Sex organs—testes and male internally  External sex organs—vagina? o At puberty—testes start to secrete higher levels of testosterone  Get male genetalia  17/18 switched gender identity  16 became heterosexual males  15 living with or married to women ▯ Sexual Orientation  Feminization/masculinization models o Brain o Hormones o Biological “markers”  Genes  Older Brothers ▯ Length of Fingers  On right hand 2D:4D ratio o Men have smaller ratio then women o Homosexual women have less than heterosexual womenww ▯ Many Questions on Sex and Gender  Know basic idea of amount of hormones before puberty, puberty, and adulthood o Postmenopausal is the highest—lacking negative feedback  What FSH and LH does in male and female  What hormone is specific in male  What hormone is specific in female o Estrogen, progesterone  Sexual behavior in rodents o Lordosis—in females  Presence and Absence of AMH and Testosterone  SRY gene  Gender Variations about the gender disorders o Genotype and phenotype of them—like CAH, AIS, and Guevedoces


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