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Motivation and the Regulation of Internal States Hunger: A Complex Drive Hunger: learning factors • Much of what we eat is culturally driven or learned – Basic food preferences (5 tastes) – Some physiological need – But mostly learning! • Learned taste aversion: – the avoidance of foods associated with illness or poor nutrition – Often occurs in one trial. • Learned taste preference – Preference for the flavor of a food – Probably developed to remember taste of food that contains a needed nutrient. – Often we choose a food based on taste, not nutrient contents! communicating about food depends on the kind of animal we are! • What is a poison or bad food? • How do humans figure out a food is rotten or poison? • How do other animals judge “bad food”- what clues do they use? • Why might we learn after only 1 experience that a food is bad- why don’t we keep eating food that made us sick? Garcia Effect or Conditioned Taste Aversion • Grp I: Tasty Water--> Nausea – Good Conditioning • Grp II: Bright Noisy Water-> Shock – Good conditioning • Grp III: Tasty Water--> Shock – No conditioning • Grp IV: Bright Noisy water--> Nausea – No conditioning A “biologicAl boundAry” • Look at the TYPE of stimuli that are being used: – Categorize each as an internal or external event • Grp I: Tasty Water--> Nausea • Internal Internal • Grp II: Bright Noisy Water-> Shock • External External • Grp III: Tasty Water--> Shock • Internal External • Grp IV: Bright Noisy water--> Nausea • External Internal • Can’t learn ACROSS modalities very well! Important Properties • Just takes once! • All animal species show it •Can remember the poison for a VERY long time! • Novel stimuli condition more readily than familiar stimuli •Different Cues for different species: • quail: color of food • monkeys: texture • rats: taste and smell •In social animals- can transmit stimulus socially Uses • Humans: dietary restrictions and smoking cessation programs (but will switch brands and tastes) • Can develop CTA with Chemotherapy- must watch pairing good food with nausea • Most important use: Wildlife Management: – Coyote management – Wolf management – Bear management keep your dog out of the garbage? • Starting and stopping eating • What starts and stops eating? Complex factors • Local theories: Cannon & Washburn – Hunger = sensation arising from gastrointestinal tract – Tied to some “sign”: • Increase in gastric juices • Full stomach – Balloon experiment: swallow balloon and fill/empty it • Subjects with filled balloon ate less, reported feeling more full • But, still ate! • Central theories: homeostatic physiological processes – Starting process – Stopping process – Selection process: what to eat and when! Process of digestion • Digestion begins in the mouth, where food is ground fine and mixed with saliva. • Saliva: – provides lubrication – contains an enzyme that starts the breakdown of food. • Digestion proceeds in the stomach: – food is mixed with the gastric juices hydrochloric acid and pepsin. – Broken down more before enters intestines • Small intestine – Receives partially processed food from stomach – Stomach releases food gradually so the small intestine has time to do its job. digestion • Duodenum – Initial 25 cm of small intestine – Digesting primarily occurs here – Carbohydrates are metabolized into simple sugars, particularly glucose. – Proteins are converted to amino acids. – Fats are transformed into fatty acids and glycerol. • Area postrema: – Area of brain outside the blood-brain barrier – Most posterior portion of brain – Exempt from blood-brain barrier functions, so toxins can activate it to induce vomiting. Phases of digestion • Absorptive phase – The few hours following a meal – body lives off the nutrients arriving from the digestive system; • Insulin release: – hormone that enables body cells to take up glucose for energy and certain cells to store excess nutrients. – The pancreas secretes during absorption phase • Storage: Some of the glucose is converted to glycogen and stored in a short-term reservoir in the liver and muscles. • Fat reserves: Any remaining glucose is converted into fats and stored in fat cells, also known as adipose tissue. Digestion phases • Fasting Phase – Eventually the glucose level in the blood drops – body must falls back on its energy stores – This is the fasting phase. • The pancreas ceases secretion of insulin – starts secreting the hormone glucagon, – glucagon causes the liver to transform stored glycogen back into glucose. • When levels are low enough, starts signals for eating again. – but; social and environmental cues can also trigger “hunger” Initiation of hunger • Three major physiological changes with hunger: – Glucopruvic hunger: low glucose signaled to brain – Lipoprivic hunger: low fatty acids – Ghrelin: neuropeptide in stomach • Liver monitors – glucose level – fatty acids in blood passing from liver to small intestine – Monitors fatty acids via hepatic portal vein • Vagus nerve carries signals from liver to NST in medulla • NST sends signals to arcuate nucleus of hypothalamus – vital hypothalamic structure – monitors the body’s nutrient condition. – This is like the thermostat in temperature regulation Initiation of hunger • The arcuate nucleus sends signals to the PVN (paraventricular nucleus) – Also part of hypothalamus- ventral medial part – initiates eating, though less effectively than the lateral hypothalamus, – regulates metabolic processes such as body temperature, fat storage, and cellular metabolism. – Modulates control via two nerotransmitters: • Neuropeptide Y (NPY); serotonin • Lateral hypothalamus: master control of eating – initiates eating – controls several aspects of feeding behavior as well as metabolic responses. Critical initiation hormones • NPY (neuropeptide Y) – – – – released from the PVN and lateral hypothalamus Released in response to signals from the arcuate nucleus dramatically increases eating But reduces metabolism. • Gherkin – Peptide that is synthesized in the stomach and released during fasting. – Also induces eating – Involved in eating disorders such as Prader Willi syndrome • 2.5 x higher in individuals with Prader Willi’s • Gherkin blocker may be an important dietary manipulation Prader Willi Syndrome • Genetic disorder: due to malfunction of cell division – caused by a gene missing on part of chromosome 15. – most patients missing genetic material on part of the father's chromosome; – others have two copies of the mother's chromosome 15. • the genetic changes occur randomly. Patients usually do not have a family history of the condition. • Symptoms – Newborns with this disorder small for gestational age; males have underdeveloped genitals – difficulties with sucking and swallowing; problems with weight gain – May seem floppy and feel like a "rag doll" when held; weak cry – Facial changes, such as "almond-shaped" eyes and a small, downturned mouth; Skin differences – Very small hands and feet compared to the body Prader Willi Syndrome • Affected children have intense craving for food; will do almost anything to get it. – results in uncontrollable weight gain and morbid obesity. – Morbid obesity may lead to lung failure – also low blood oxygen levels, right-sided heart failure, and death. • Signs and tests – Abnormal glucose tolerance – Above normal level of the hormone insulin in the blood – Failure to respond to luteinizing hormone releasing factor – High carbon dioxide levels; low oxygen • Obesity is the greatest threat to health. Prader Willi Syndrome Manipulating onset of eating • Stopping eating: Blocking NPY or gherkin or damage to LH or PVN greatly disrupts eating • Starting/maintaining eating: Injections of NPY into PVN results in huge increase in eating – Rats may gain 6x or more body weight – Can also induce by lesioning PVN – Really can’t stop eating! • During extreme deprivation: NPY reduces metabolism and increases motivation to eat – By decreasing metabolism, conserve body fat/glucose stores – At same time, make animal more active, thus more likely to get food – Also suppresses sexual behavior• Again conserves energy • Also lessens chances of producing nonviable offspring Signaling an end to a meal • Mouth factors: – Full mouth – Chewing – Learning • Stomach factors – Full stomach is a cue to stop – Phillips and Powley (1996): • Inflated cuff to close off stomach/duodenum • Infused glucose into stomach • Infused saline into stomach • As long as stomach felt “full” – ate less • Also respond to caloric intake – High calorie soup produces greater reduction in eating than low-calorie soup – Issue of diet drinks: may eat MORE when drink diet drinks- not get satiety signal • Optimal factor: mouth+stomach+intestines signal to brain Signaling an end to a meal • Stomach and intestines respond to food by releasing various peptides that brain uses to monitor intake – – – – Some peptides respond to carbohydrates Some to fats Some to proteins Some to mixes • Peptides induce pancreas, liver, gallbladder to secrete appropriate enzymes indo duodenum – Allows appropriate digestion of specific nutrients – Signal to brain which nutrients digested via vagus nerve or bloodstream Satiety hormones • CCK (cholecystokinin) – The best known of the satiety signals – a peptide hormone that is released as food passes into the duodenum. – CCK detects fats and causes the gall bladder to inject bile into the duodenum, which breaks down the fat so it can be absorbed. – Relatively short term regulation • PYY (peptide YY3-36) – Another appetite-suppressing peptide hormone – released in the intestines in response to food – carried by the blood stream to the arcuate nucleus; inhibits the NPYreleasing neurons. – Note: non-neural route to the brain thus action is too slow to limit the current meal; – instead it decreases calorie intake by about a third over the following 12 hours. – LONG term regulation Satiety hormones • leptin. – – – – – Fat cells secrete leptin inhibits eating The amount of leptin in the blood proportional to body fat. Leptin helps regulate meal size, Regulates in response to long-term stores of fat rather than the nutrients contained in the meal. • Can demonstrate effect of these hormones: VMH lesions (much like Prader Willi’s syndrome) – Increase parasympathetic activity in vagus nerve – Enhances insulin release – Creates persistent absorption phase in which more nutrients are stored rather than used – Animal MUST overeat to maintain normal energy level – BUT: also becomes obese because of huge storage