Motivation and the Regulation of Internal States Hunger: A Complex Drive

1. Motivation and the Regulation of Internal States Hunger: A Complex Drive

2. 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!

3. 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?

4. 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

5. 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 • InternalInternal • Grp II: Bright Noisy Water-> Shock • ExternalExternal • Grp III: Tasty Water--> Shock • InternalExternal • Grp IV: Bright Noisy water--> Nausea • External Internal • Can’t learn ACROSS modalities very well!

6. 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

7. 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

8. keep your dog out of the garbage?

9. 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!

10. 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.

12. 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.

13. Phases of digestion • Absorptive phase • Thefew 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.

14. 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”

15. 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

16. Initiation of hunger • Thearcuate 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.

17. 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 PraderWilli syndrome • 2.5 x higher in individuals with PraderWilli’s • Gherkin blocker may be an important dietary manipulation

18. PraderWilli 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

19. PraderWilli 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.

20. PraderWilli Syndrome

21. 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

22. 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

23. 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

24. 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 NPY-releasing 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

25. 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 PraderWilli’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