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Psyc6 week 6

by: Sabrina Straus

Psyc6 week 6 PSYC 6

Sabrina Straus

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About this Document

class notes and chapter notes motivation
Introduction to Neuroscience
Catherine Cramer
Class Notes
PSYC, neuroscience, motivation
25 ?




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Popular in Psychology (PSYC)

This 3 page Class Notes was uploaded by Sabrina Straus on Tuesday October 18, 2016. The Class Notes belongs to PSYC 6 at Dartmouth College taught by Catherine Cramer in Fall 2016. Since its upload, it has received 2 views. For similar materials see Introduction to Neuroscience in Psychology (PSYC) at Dartmouth College.


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Date Created: 10/18/16
3. 10-17-16 Intro to Neuro class notes + Chapter notes MOTIVATION: HOMEOSTASIS ~behavioral action depends on lateral hypothalamus Terms ● Prandial state: blood is filled w/ nutrients ● Anabolism: assembly of macromolecules ● post absorptive state: fasting between meals ● Catabolism: breaking down complex macromolecules ● Lipostatic hypothesis: brain monitors amy of body fat ~idea of balance ~unconscious (sensory stimulation)->conscious (neurons of frontal lobe) I. Homeostasis - set point: temp, drive​} by hypothalamus -cells are sensitive to temp esp anteriorhypothalamus >cold->TSH (anterior pituitary)->constrict blood vessels and goose bumbs >hot->reduce TSH-> blood is shunted toward periphery to dissipate heat ~responses >humoral: respond to sensory signals by stimulating or inhibiting release of pituitary hormones >visceromotor:adjust balance of sympathetic and parasympathetic outputs or autonomic nervous system >somatic: (esp in lateral hypothalamus) incite somatic motor behavioral response A. Local (peripheral) factors: core trumps peripheral B. Central factors II. Thermoregulation A. Local factors - skin temperature B. Central factors: sensors in hypothalamus anterior hypothalamus - "heat detectors" of blood-> cooling mechanisms posterior hypothalamus - "cool detectors" of blood-> heating mechanisms ~thermostat and editing in hypothalamus } behavior and physiological response III. Thirst systems: triggered by lateral hypothalamus A. Fluid “compartments” 1. Extracellular (EC) = blood + interstitial fluid ~loose blood by salinity doesn’t change} tenicity -hypertonic: more salt in fluid-> fluid goes out to try to offset excess salt-> cell volume ​ sensed by vascular organ of the lamina terminalis=water leaves cells by osmosis-> OVLT neurons directly excite magnocellular neurosecretory cells to secrete vasopressin and stimulate osmometric thirst >Hypovolemic thirst: to little volume in extracellular -> drink salty/isotoni​ decrease blood volume >Osmotic: too little in cell -> drink water ~can over inflate cells if you drink too quickly 2. Intracellular (IC): inside all cells B. Maintaining volume 1. Kidney function - reabsorption Vasopressin-increase water retention{ ​ ypovolemia->reduce blood flow to kidney-> 2. Function and mechanism of aldosterone release renin -> angiotensin I -> angiotensin II-> want to eat salt, retention of water, increase in blood pressure Reduced blood flow to kidneys->rise of angiotensin II->stimulate neurosecretory cells to release vasopressin-> constrict arterioles and need for thirst } diabetes=replace vasopressin ~hyper->pee out 3. Function of antiduiretic hormone (ADH = vasopressin) C. Thirst induction via extracellular challenge (hypovolemic thirst) -> cardiac+Kidney-> hypothalamus-> thirst and more blood flow D. Thirst induction via intracellular challenge (osmotic thirst) : thirst-> OVLT-> supraoptic nucleus, paraventricular nucleus-> water conservation w/ release of vasopressin E. Brain areas involved in thirst subfornical organs OVLT and osmosensory neurons: detect own size OVLT-> neurosecretory cells->posterior pituitary w/ vasopressin and to lateral hypothalamic area for drinking Lateral preoptic area (of hypothalamus)-> if removed rat would stop drinking when osmotically thirsty IV. Metabolic processes​}important for storage / in lateral hypothalamus Steps to eating Cephalic: sight and smell of food-> secretion of saliva Gastric phase: actual eating Substrate: food is digested and moved to intestines while nutrients go into bloodstream A. Absorptive phase - storage } sugar, fat, and amino acids-> energy, protein synthesis, and storage Triglycerides} long term -> fat and glycerol and glucose-> Glycogen} short term in liver-> glucose >glucose->brain >fat->muscle Food consumption-> satiety->orexigenic->eat B. Fasting phase - conversion of stored nutrients to useful forms } satiety V. Theories of feeding control A. Glucostatic theories 1. Insulin and glucagon >insulin moves glucose into non neuron cells for use or storage} ​ released by pancreas/ important for anabolic metabolism(stored) and catabolic (released) -low insulin: rise blood glucose levels -rises during cephalic phase and increases further during gastric phase} at max when food is absorbed-> high insulin and blood glucose tells body you are full} acts directly on arcuate and ventromedial nuclei >glucagon when levels are low-> storage in converted to glucose } slows return of hunger 2. Site of glucoreceptors Hepatic (liver): 1st to know / respond to changes by sending neurosignals through vagus nerve } info from liver has more importance ~if you cut vagus nerve the brain can still detect glucose Central - hypothalamus ~eating: body monitors to base line B. Lipostatic theories Ventromedial hypothalamic syndrome: eat a lot -> change set point Lateral hypothalamic syndrome: lesions=don’t eat Leptin-​fights obesity}rise when body fat increases->deficiency results in hunger} informed to cortex by MCH (prolongs consumption) Orexin: also stimulates feeding and rises when leptin falls} promotes consumption and wakefulness C. More peripheral factors 1. Gastric (stomach) factors:​ distension/stretching-> axons go thru vagus nerve to tell brain you are full->nucleus of solitary tract in medulla} stomach Ghrelin​:strongly stimulates appetite and food consumption by activating NPY/AgRP 2. Duodenal factors Cholecystokinin (CCK): ​ inhibits meal frequency and size} caused by fats-> gastric distension} in cells that line intestine 3. "Head" factors (e.g., taste, flavor, mouth-feel, experience, timing) VI. Integration and redundancy Arcuate nucleus: ​activated by rise in leptin contain aMSH and CART NPY/AgRP neurons: ​ inhibit secretion of TSH and ACTH-> activate parasympathetic division and stimulate feeding} orexigenic peptides bc low leptin -fall in leptin->release arcuate nucleus neurons and MCH+orexin from lateral hypothalamic area -stimulate feeding and decrease metabolism POMC/aMSH/CART neurons: ​trigger humoral response by triggering paraventricular nucleus-> diminish appetite}anorectic peptides bc high leptin -rise leptin->release -inhibit feeding and increase metabolism Disorders: accompanied by abnormalities of serotonin >anorexia nervosa >bulimia: eating binges


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