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Lecture 10: Hunger and Thirst

by: Rachael Couch

Lecture 10: Hunger and Thirst NSC 3361

Marketplace > University of Texas at Dallas > Neuroscience > NSC 3361 > Lecture 10 Hunger and Thirst
Rachael Couch
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About this Document

This week's notes: in-class, lecture slides, and clicker questions in organized word format
Behavioral Neuroscience
Van S Miller
Class Notes
behavioral neuro, Neuro, nsc, 3361, UTD, Miller, van miller
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This 5 page Class Notes was uploaded by Rachael Couch on Tuesday February 16, 2016. The Class Notes belongs to NSC 3361 at University of Texas at Dallas taught by Van S Miller in Summer 2015. Since its upload, it has received 56 views. For similar materials see Behavioral Neuroscience in Neuroscience at University of Texas at Dallas.

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Date Created: 02/16/16
Lecture 10: Hunger and Thirst Homeostatic systems ­ Negative feedback systems are the main homeostatic mechanisms o Defending/maintaining a set point Thirst ­ Hypovolemic thirst o Stimulated by low extracellular/intravascular volume (loss of water volume)  Ex: sweating, bleeding (salt and water is lost in these cases) o Water is stored in the blood stream and the extracellular space   Low volume in these areas = reduced blood pressure  Salt concentration is not changed o 1) Baroreceptors detect the initial drop in blood pressure  Activate the angiotensin cascade o 2) If blood volume decreases, the kidneys release renin, which triggers formation  of angiotensin II  Angiotensin II  is the most potent hormone in the human body o 3) Release of angiotensin II triggers 3 main effects  Arteries constrict to raise BP temporarily until salt/water can be replaced  Release of vasopressin (antidiuretic hormone)  Induces blood vessel constriction to reduce blood flow to the  bladder  Circumventricular organs trigger drinking  Circumventricular organs are located around the ventricles  They measure the salt concentration and volume of CSF produced  by the ventricles  2 major circumventricular organs: SFO and OVLT o Subfornical organs (SFO) – signals other brain sites to  drink when it receives angiotensin II  If SFO the SFO cut out, an animal would die of  dehydration with water 10 ft away from them  because they don’t feel thirsty  o Summary of effects:   Loss of volume (water and salt)  dec. BP  renin  inc. in angiotensin II   thirst, constriction of vessels (raised BP), and reduced flow to bladder  Clicker question: A fall in blood angiotensin levels does not occur after  eating salt, make one feel thirsty, or raise BP   Thirst and raised BP result from increased angiotensin II  Eating salt changes the osmolarity and is related to osmotic thirst  which is not controlled by angiotensin II o Problems  Pituitary adenoma – too much vasopressin   Diabetes insipidus ­ vasopressin is not produced, kidneys send more urine  to the bladder resulting in chronic thirst ­ Osmotic thirst  o Stimulated by high extracellular solute concentration (increased blood osmolarity)  Salt is added to the blood, cannot come in so water goes out to dilute it  Water leaving the cell causes the cell to shrink o All foods have osmos (salt/sodium)  Eating  high sodium concentration (makes neurons more likely to fire)   After eating, we have to drink to return to homeostasis  o 1) Mechanoreceptors sense osmolarity by sensing how “stretched” the blood  membranes are o 2) Osmosensory neurons in the anterior hypothalamus (OVLT) respond to a rise in blood osmotic pressure   Their cell membranes shrink and open Na  channels  This causes the pituitary to release antidiuretic hormone o Other related “sensing” area: area postrema ­ How does the body know to stop drinking? o Distension of stomach and intestines, cooling and moistening of mouth,  rehydration of blood Hunger  Energy utilization ­ Glucose ­ principal fuel for energy  o The brain can only use glucose while other organs can use glucose, AA, fat,  glycogen, etc. o Basis of the Atkins/ketogenic diet – brain forced to use ketones (from fat) by  eating almost nothing but fat; useful for treating seizures  ­ Glycogen ­ glucose stored for short term in the liver ­ Glycogenesis­ converts glucose to glycogen, using insulin ­ Lipids – fat tissue for long­term storage Hunger signaling ­ Much more complicated than thirst; 100s of signals are integrated to control hunger o The brain integrates all the signals to decide hunger o Possible reason for obesity – problem in integrating signals; weighing the hungry  signals more heavily ­ Pro­hunger signals: ghrelin, cortisol, NPY, AgRP ­ Anti­hunger signals: leptin, glucose, insulin, PMC, CART, norepinhephrine ­ External factors – emotions, food characteristics (desirability), lifestyle behaviors  (adaptation to habits – “breakfast eater” or not), environmental cues (more difficult to  diet when at a restaurant, cold induces hunger) ­ Central (brain) signals o Neurotransmitters (dynorphin, norepinephrine, CART) o Some stimulate and some inhibit (CART)  ­ Leptin o Produced and secreted into the bloodstream by fat cells o Levels are measured by the hypothalamus o Defects in leptin production or sensitivity give a falsely low report of body fat  causing overeating and obesity ­ Ghrelin o Appetite stimulant o Released by stomach endocrine cells  o Rise/fall several times per day o Some obese people have elevated ghrelin levels ­ Hypothalamus is the hunger control center o Lateral hypothalamus (LH) encourages eating, involved in controlling set point  When the LH is damaged in animals, they stop eating  After repaired, they resume eating but stabilize their weight at a new,  lower level (new set point)  o Ventromedial hypothalamus (VMH) encourage animal to stop eating, involved  in controlling set point  When the VMH is damaged in animals (lesions), they overeat until they  become obese  Once VMH is repaired, they level to a higher weight   Don’t go back to normal, they have a higher set point  o LH and VMH connect to the PVN (periventricular nucleus) which integrates the  signals  o Arcuate nucleus in hypothalamus contains 2 sets of opposing neurons:  NPY/AgRP neurons  Produce neuropeptide Y and agouti­related peptide  Stimulate appetite and lower metabolism  weight gain  Leptin inhibits secretion of AgRP (blocks weight gain)  PMC/CART neurons  Produce pro­opiomelanocortin and cocaine­ and amphetamine­ related transcript (CART)  Inhibit appetite and raise metabolism  weight loss o Drugs and exercise raise the metabolism  Eating Disorders Anorexia Nervosa  ­ Refusal to maintain body weight o Continually lowering set point – no amount of weight loss will be enough ­ Fear of weight gain ­ Body image disturbance (brain perception problem/brain disorder) ­ Amenorrhea ­ stop having periods; body goes into anti­reproductive mode because the  body doesn’t have enough food to support two people ­ Restricting or binge­eating/purging type ­ Highest mortality rate of any psychiatric disorder ­ 0.5% lifetime prevalence in women  (.05% in men) ­ Other symptoms of anorexia o Thinning of the bones, brittle hair and nails, dry and yellowish skin, mild anemia,  muscle weakness and loss, lethargy, severe constipation, low blood pressure,  slowed breathing and pulse, drop in body temperature ­ Teenage girls with anorexia have a  o larger insula, a part of the brain that is active when you experience disgust o larger orbitofrontal cortex, part of the brain that tells you when to stop eating ­ Other psychiatric conditions o Anorexia almost never occurs by itself o Of women with anorexia or bulimia – 90% have depression, large percentage  have childhood anxiety disorders, OCD, or abuse alcohol or drugs o 30% of women with an eating disorder attempted suicide, 5% died ­ Kids’ Eating Disorders Survey (KEDS) o Grades 5 to 8: 30% dieting, 10% fasting, 5% vomiting Bulimia ­ Not the same thing as anorexia  ­ Recurrent binge eating; recurrent inappropriate compensatory behavior; at least 2x/wk for 3 months Obesity treatment ­ Eating less (daily deficit of 500­1000 calories) ­ Modifying behavior to avoid temptation (lifestyle change) ­ Strenuous and frequent exercise o Moderate exercise has minimal effect on weight loss ­ Alternative therapies include… o CB receptor antagonist o Treating obesity as an addiction  Obese people have fewer dopamine D2 receptors and lower prefrontal  lobe metabolism o Altering metabolism o Gastric bypass therapies  Weight loss averages 25% and is long­lasting  Reducing hunger by reducing ghrelin and increasing inhibitory signals Metabolism ­ Basal metabolic rate (BMR): energy required to fuel the brain/body and maintain  temperature ­ At the start of a diet, the basal metabolic rate will fall – to prevent losing weight o Starvation – the body compensates to save energy – “survival mode” ­ Controls 75% of energy expenditure  ­ Low BMR  failure to lose weight ­ Heredity accounts for 40% of a person’s BMR. But, spontaneous activity can increase it Case Studies Case Study: Izzy  ­ Throughout his later life Izzy was obese, at one point carrying 757 pounds ­ At age 38, he died of heart failure in 1997 ­ Obesity is a brain disorder – derangement in homeostasis  Case study: Kate Kane ­ Food is on her mind "all the time"; "I could eat until I die, basically" ­ Kate, 26, has Prader­Willi syndrome, ­ Ghrelin levels are elevated in Prader­Willi ­ Feels so hungry that she begs, steals and even eats out of the garbage to get to food, if  someone doesn’t stop her


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