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Quiz 8

by: jjb13n

Quiz 8 PSB 3004C

GPA 2.54

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About this Document

Material needed for quiz 8
Physiological Psychology
Dr Hull
Study Guide
50 ?




Popular in Physiological Psychology

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This 5 page Study Guide was uploaded by jjb13n on Friday March 11, 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 18 views. For similar materials see Physiological Psychology in Psychlogy at Florida State University.

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Date Created: 03/11/16
Quiz 8 Study Guide    ● What two kinds of cues can trigger thirst?    ○ Hypovolemic Thirst (reduced extracellular volume)  ○ Osmotic Thirst (high extracellular solute concentration)  ● What are 2 functions of vasopressin when body fluids are low?  What is its other  name?  What is diabetes insipidus?  ○ Reduces fluid loss at the kidney (by inserting aquaporins in the collecting ducts of  the kidneys)  ○ Constricts blood vessels, and the formation of angiotensin II, which acts on the  brain to trigger thirst, constricts blood vessels, and stimulates vasopressin release  ○ Vasopressin aka ADH (antidiuretic hormone)  ○ Diabetes insipidus (no vasopressin → kidneys retain less water → chronic thirst)  ● What is hypovolemia and why is it dangerous? How is it detected by the body?  ○ Release of vasopressin (a.k.a. antidiuretic hormone, ADH) from posterior  pituitary → blood vessel constriction and increases water retention by the kidney  ○ Baroreceptors in blood vessels and the heart detect the initial drop  ● Why is it necessary for the kidney to have sufficient blood pressure?   ○ Kidneys need enough blood pressure to squeeze plasma out of blood vessels to  form urine & excrete metabolic waste   ● Summarize briefly how the kidney works.  ○ The kidney filters and conserves body fluid.   ○ It requires sufficient blood pressure to extrude plasma out of the capillaries in the  glomeruli.   ○ That plasma would be lost as urine if it is not reabsorbed back into the body.   ○ Cells lining the loop of Henle in the kidney pump Na+ out of the fluid and back  into tissue around the loop. Cl­ follows Na+ passively, due to electrical attraction.   ○ Water follows passively, due to osmosis. The water passes through aquaporins,  small channels in the collecting ducts of the kidney. ~99% of filtered fluid is  conserved in this way  ● What leads to the production of angiotensin II, and what are 2 of its main effects?  What are 2 brain areas that respond to angiotensin II?  ○ When blood volume is low, the kidney releases renin  ■ Renin converts angiotensinogen to angiotensin I, which is converted to  angiotensin II by angiotensin converting enzyme (ACE)  ○ 2 main effects:  ■ Constricts blood vessels (conserves water)  ■ Releasing vasopressin and aldosterone  ○   2 brain areas ­­­>Subfornical organ and preoptic area  ● What is osmotic pressure? What happens if you pour salt into one side of a  container that is separated from the other side by a semipermeable membrane?  ○ Osmotic pressure moves water across a membrane, along its concentration  gradient  ○ Water flows through the membrane, equalizing the solute concentrations and  shrinking the cell; salt can’t cross the membrane  ● What is the major role of the OVLT in osmotic thirst?  ○ OVLT (a brain area adjoining the 3rd ventricle)  ● Why is it beneficial to have enough salt in the body in order to respond to  hypovolemia?  What hormone promotes Na+ conservation?  ○ Salt is needed to maintain water in the extracellular compartment; important for  fluid balance  ○ Aldosterone  ● What is the effect of insulin on blood glucose?  What is the effect of glucagon?  ○ Insulin regulates the process of converting glucose to glycogen  ○ Glucagon, another pancreatic hormone, → glycolysis ­ converts glycogen back  into glucose when blood levels drop  ● Why do people with untreated diabetes I eat a lot but gain little weight?  ○ Their pancreas stops producing insulin  ■ No insulin = no fat storage  ● Where is leptin produced?  Why can’t we treat most obese people with leptin?  ○ Leptin is released from fat cells in adipose tissue and secreted into bloodstream  ○ Because most obese people lack either the leptin receptor or leptin itself  ● What is the evidence that the lateral hypothalamus (LH) is important for hunger?  ○ Lateral hypothalamus (LH) lesions caused aphagia—refusal to eat – it was  identified as a hunger center.  ● What behavioral changes are produced by lesions of the ventromedial  hypothalamus (VMH)?  ○ VMH­lesioned animals exhibit a dynamic phase of obesity with hyperphagia  (overeating) until they become obese  ○ They are also finicky—eat only palatable food  ● Why do we not think that animals with VMH lesions are simply ravenously hungry  all the time?  ○ It isn’t so much that the rats are getting fat because they are eating too much ­­  they are eating too much because they are getting fat!!!  ● What is the function of the paraventricular nucleus (PVN) in controlling eating?  What nucleus controls the PVN?  ○ Integrate appetite signals & modulate food intake  ■  NPY/AgRP (neuropeptide Y) and (agouti­related peptide)  ○ Arcuate nucleus  ● What is leptin? Which brain nucleus responds to leptin?   ○ Leptin activates POMC/CART neurons but inhibits NPY/AgRP neurons, so leptin  suppresses hunger  ○ Arcuate nucleus of the hypothalamus  ● When and where is ghrelin produced?  What is its effect on feeding?  ○ Ghrelin is released into the blood by endocrine cells in the stomach  ○ Besides stimulating growth hormone release (where it gets its name), ghrelin is an  appetite stimulant.  ○ Ghrelin increases the release of glucose from the liver; however, that glucose  can’t be used for growth unless somatomedin is also released from the liver. If  someone is hungry, somatomedin is not released. Therefore, the glucose →  metabolism.  ○ Levels of ghrelin rise during fasting and fall after a meal, except in obese subjects  – they remain high.  ○ Ghrelin and PYY3­36, acting mainly on NPY/AgRP neurons, work in opposition  to provide short term appetite control.  ○ Ghrelin stimulates the cells, leading to an increase in appetite  ● What is one physiological way in which lesions of the VMH promote obesity and one  way in which the LH contributes to feeding?  ○ Higher set zone for weight  ○ Lower set zone for weight  ● What is the effect of alpha­MSH on hunger?  How about neuropeptide Y (NPY)?  How about endocannabinoids?  ○ α­MSH inhibits the LH’s appetite­ stimulating activity, resulting in less feeding  ○ NPY/AgRP neurons activate the PVN and LH, increasing feeding  ○ Endocannabinoids  –  homologs of marijuana – increase appetite and feeding  ● What are some possible treatments for obesity?  ○ Leptin for a tiny minority who lack it. (Most have lots of leptin but have  insensitive receptors for it.)  ○ Cannabinoid antagonists  ○ Alpha­MSH agonists (also prosexual)  ○ Certain thyroid agonists  ○ Angiogenesis inhibitors  ○ Reducing fat absorption (bad side effects)  ○ Reduced reward  ○ Anti­obesity surgery (gastric bypass > fat removal)  ● Compare the symptoms of anorexia nervosa with those of bulimia nervosa and  binge eating.  ○ Anorexia  ■ Refusal to maintain body weight (BW) at or above a minimally normal  weight for age and height.  ●   BW < 85% of normal   ●   BMI < 17.5 kg/m2  ■  Intense fear of gaining weight or becoming fat.  ■ Disturbance of body image.  ■ Amenorrhea (primary or secondary).  ○ Bulimia  ■ Marked by periodic gorging and purging by vomiting or laxatives  ○ Binge Eating  ■ Gorging with more food than is necessary to satisfy hunger                                                                        


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