Motivation and the Regulation of Internal States Chapter 6

1. Motivation and homeostasis Hunger: a complex drive Obesity Anorexia and bulimia Motivation and the Regulation of Internal StatesChapter 6

2. Motivation and Homeostasis • Motivation means “to set in motion;” it refers to the factors that initiate, sustain, and direct behaviors. • Theoretical Approaches to Motivation • Instinct: a complex behavior that is automatic and unlearned, and occurs in all members of a species, such as maternal behavior. • Instincts account for few if any behaviors in humans. • Drive theory: The body maintains homeostasis—equilibrium—in its systems. • Departure from homeostasis produces an aroused condition, or drive, impelling the individual to engage in appropriate action.

3. Motivation and Homeostasis • Incentive theory: People are motivated by external stimuli, or incentives, not just internal needs. • Incentives include money, grades, the smell of food. • Arousal theory: People behave in ways that keep them at their preferred level of arousal. • This is a factor, for example, in the characteristic of sensation seeking. • In response to challenges to drive theory, psychologists have shifted to an emphasis on drives as states of the brain rather than as conditions of the tissues. ◊

4. Motivation and Homeostasis • Simple Homeostatic Drives: A “control system” maintains conditions around a set point. • Temperature Regulation • Ectotherms, such as reptiles, cannot regulate body temperature internally. • Endotherms regulate their body temperature by dilating or constricting blood vessels, adjusting metabolism, sweating, etc. • Warmth-sensitive and cold-sensitive cells in the preoptic area of the hypothalamus receive input from the blood and the skin. • The preoptic area initiates temperature regulating responses.

5. Motivation and Homeostasis • Thirst is more complicated in that it involves two kinds of deficits and two different systems. • Osmotic thirst occurs when the fluid content decreases inside the cells. Water is drawn from cells into the bloodstream, usually to compensate for food intake. • Detected in the hypothalamus by the OVLT(near 3rd ventricle). • The OVLT signals the median preoptic nucleusto initiate drinking. ◊

6. Motivation and Homeostasis • Hypovolemic thirst occurs when blood volume drops, due to a loss of extracellular water. • Caused by sweating, vomiting, diarrhea, blood loss, etc. • Lowered blood volume is detected by receptors in the heart and in the kidneys. • Information from the heart is relayed by the vagus nerve to the nucleus of the solitary tract and to the median preoptic nucleus. • The kidneys release the hormonerenin; • which increases production of angiotensin II; • which stimulates thesubfornical organ; • which signals the median preoptic nucleus.

7. Thirst Control Signals and Brain CentersFigure 6.3

8. Hunger: A Complex Drive • Hunger: Feeding behavior must provide energy for fuel and for maintaining body temperature, as well as material needed for growth and repair. • Five primary tastes help select safe and nutritious foods. • Naturally sweet foods tend to be nutritious. • Salty foods provide ions necessary for neural transmission. • Sour foods may be spoiled, and bitter foods may be toxic. • Umami taste may help select proteins. • Receptors in the tongue’s taste buds send signals to theinsula (the primary gustatory cortex), and to thenucleus of the solitary tract(NST).

9. Papilla with Taste BudsFigure 6.4

10. Hunger: A Complex Drive • Sensory-specific satiety occurs when a food becomes less appealing as the individual consumes more. • This encourages variation in food choices for a balanced diet. • This type of satiety involves the NST in the medulla. • Learned taste aversion is the avoidance of foods associated with illness or poor nutrition. • Examples: bait shyness, avoidance of a nutrient-deficient diet • Learned taste preference is a preference for the flavor of a food that contains a needed nutrient. • This ability is often counteracted by the distraction of tasty, high-calorie foods not found in nature.

11. Hunger: A Complex Drive • Digestion • Digestion begins in the mouth, where an enzyme in saliva starts the break down of food. • In the stomach, food is mixed with hydrochloric acid and pepsinto further digest food. • Most of digestion takes place in the small intestine, particularly in theduodenum(initial 25 cm). • The products of digestion (glucose, amino acids, fatty acids and glycerol) are absorbed through the intestinal walls. • These nutrients are transported to the liver by thehepatic portal vein. ◊

12. The Digestive System Figure 6.6

13. Hunger: A Complex Drive • The feeding cycle has two phases: • During theabsorptive phase, the body uses the nutrients arriving from the digestive system. • Rising glucose levels activate the parasympathetic system, which promotes the release of insulin. • In cells outside the nervous system, insulin receptors activate glucose transporters to carry glucose into the cells. • The transporters in the nervous system do not require insulin; this gives the brain priority access to glucose. • Nutrients are also stored for future use during this phase. • Glucose is stored as glycogen in the liver and muscles. • Excess glucose is converted into fats and stored in adipose tissue.

14. Hunger: A Complex Drive • During thefasting phaseglucose levels have fallen, and the body must rely on stored nutrients. • The sympathetic nervous system promotes the release of glucagon, which converts the liver’s glycogen to glucose. • Because insulin levels are low, this glucose is available only to the brain. • Glucagon, secreted by the pancreas, breaks stored fat down into fatty acids and glycerol. • Fatty acids are used by the muscles and organs. • Glycerol is converted to glucose for the brain. ◊

15. Hunger: A Complex Drive • Cycles of feeding and fasting are mostly choreographed by: • the lateral hypothalamus, which initiates eating and • controls several aspects of feeding and metabolic responses. • the parventricular nucleus, which has metabolic functions.

16. Hunger: A Complex Drive • Signals That Start a Meal • There are three major signals for hunger: • glucose deficit, which triggers glucoprivic hunger; • a deficit in fatty acids, which triggers lipoprivic hunger; • release of ghrelin as the stomach empties. • The first two signals are carried by the vagus nerve to theNST (nucleus of the solitary tract) in the medulla. • Ghrelin reaches the NST via the bloodstream. ◊

17. Hunger: A Complex Drive • The NST then communicates this informationto thearcuatenucleus in the hypothalamus. • The arcuate nucleus sends neurons to the lateral hypothalamus and the PVN. • These neurons releaseneuropeptide Yand agouti-related protein (AgRP), • which excite the lateral hypothalamus and the PVN to increase eating and reduce metabolism. ◊

18. Hunger: A Complex Drive • Signals That End a Meal • Satiety signals are essential to end a meal long before the nutrients reach the body’s tissues. • Stretch or volume receptors in the stomach signal meal size. • The stomach and intestines release different peptides in response to different types of food, and at least some of them act as signals in the brain. • The best known of these peptides ischolecystokinin(CCK), which is released as food passes into the duodenum. • It detects fats and aids in fat digestion by causing the gall bladder to release bile. • CCK stimulates the vagus nerve; the signal travels to the NST and from there to the hypothalamus to decrease eating.

19. Hunger: A Complex Drive • Long-term control of appetite is also essential. • The intestines releasePYY (Peptide YY3-36), which is carried by the bloodstream to the arcuate nucleus where it inhibits NPY-releasing neurons. • Fat cells releaseleptin. • Leptin provides a fat level/body weight monitor. • Along with insulin, it inhibits hunger-inducing AgRP. • It also activates POMC/CART, substances that reduce feeding by inhibiting the PVN. • It helps regulate meal size on a long-term basis. ◊

20. Hunger Control Signals And Brain Centers Figure 6.8

21. Obesity • Obesity: • is defined as a BMI (body mass index) of 30 or higher. (over 40: morbidly obese; 25-29 overweight) • has doubled in the U.S. since 1980 and has become a global epidemic; • is associated with a variety of diseases, including diabetes, heart disease, high blood pressure, stroke, and colon cancer; • is also linked to temporal lobe shrinkage, cognitive decline, and risk of Alzheimer’s disease; • threatens to reduce average lifespan. (Caloric restriction increases lifespan, and research is focused on drugs that accomplish the same thing.)

22. Obesity • The Contribution of Heredity • The heritability of obesity ranges from 50-90%. • Adopted children’s weight and BMIs are moderately related to those of their biological parents, but have little similarity with those of their adoptive parents. • Around 200 genes have been implicated in obesity; two dozen of these are specific to humans. Examples: • Obesity (ob) gene on chromosome 4 • Diabetes (db) gene on chromosome 6 • Mutations in the MC4R gene • FTO gene (A allele)

23. The ob/ob Mouse in on the RightFigure 6.16

24. Obesity • Obesity and Reduced Metabolism • Basal metabolic rate (BMR): • is the energy required to fuel the brain and body and maintain temperature; • accounts for 75% of energy expenditure in the average sedentary person. • In a study of women on a restricted diet, the 1/3 who failed to lose weight had lower BMRs. • Heredity accounts for 40% of a person’s BMR. • The body will “defend” its weight by shifting metabolism. • This defense is less for weight gain than for weight loss. • Prolonged weight gain may shift the set point higher. • Spontaneous activity may be as important as BMR in resisting obesity.

25. Obesity • Treating Obesity • Dietary restriction works, especially when coupled with exercise to burn calories and adjust metabolism. • Medication has not produced encouraging results. • Drugs that inhibit serotonin reuptake (Ex: sibutramine) reduce carbohydrate intake, but only in people with carbohydrate craving. • Leptin reduces weight only in the 5%-10% who are leptin deficient. • Orlistat (blocks fat absorption) and exenatide (increases insulin) have significant side effects, and PYY may be ineffective.

26. Obesity • Another approach is to treat obesity as an addiction. • Obese people share several characteristics with addicts. • They have reduced numbers of dopamine D2 receptors and associated decreases in prefrontal metabolism. • Peptides that induce eating target dopamine neurons. • Anti-addiction drugs are showing effectiveness in weight loss. Figure 6.20: Reduced dopamine receptors in obesity

27. Obesity • Gastric bypass surgery is an option for the morbidly obese. • Weight loss averages 25% after 10 years, compared to 5%-10% with dieting and, most often, relapse within a year. • Reduces ghrelin and increases PYY and GLP-1, reducing hunger. • Benefits include reduced mortality and many health improvements. ◊

28. Gastric Bypass SurgeryFigure 6.21

29. Anorexia and Bulimia • Anorexia nervosa is known as the “starving disease.” • The individual restricts food intake to maintain weight at a level so low that it is threatening to health. • Restrictorsrely only on reducing food intake to control their weight. • Purgersrestrict their calorie intake, but they also resort to purging, by vomiting or using laxatives. • The anorexic individual may actually be battling hunger; NPY and ghrelin levels are high and leptin levels are low. ◊

30. Anorexia NervosaFigure 6.22

31. Anorexia and Bulimia • Bulimia nervosa also involves weight control, by bingeing and purging. • If the bulimic restricts food intake, it is only for a few days at a time, and restricting takes a backseat to bingeing and purging. • Forty-four percent overeat, but most are of normal weight. • Bulimics also may be battling hunger: • ghrelin levels decrease less following a meal; between meals they are a third higher than in controls; • PYY levels rise less following a meal. ◊

32. Anorexia and Bulimia • Environmental contributions play a role in anorexia and bulimia. • One factor is the emphasis on thinness, as seen in the Fiji study. • The incidence is higher in females, who experience more pressure. • Genetic influence is suggested by: • shared disorders in relatives and • comorbidity with obsessive-compulsive disorder (anorexia) and depression (bulimia). ◊

33. Anorexia and Bulimia • Both anorexics and bulimics show alterations in serotonin levels. • Serotonin is low in bulimics; antidepressants, which increase serotonin activity, provide some symptom improvement. • Serotonin is low in purging anorexics while ill and rises to normal after weight gain. Their personality characteristics suggest low serotonin, and drugs that reduce serotonin impair treatment. • Restricting anorexics have high serotonin after weight gain, which is typical of people with obsessive-compulsive disorder. • But dopamine may also be involved. Olanzapine, an anti-schizophrenic drug that blocks dopamine receptors, produces some benefit.