Motivation 1 of 6. during the prandial state when the blood is filled

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1 Motivation 1 of 6 I. INTRODUCTION A. Motivation: a condition (usually internal) that initiates, activates, or maintains goal-directed behavior. B. Archery analogy 1. undrawn bow has no potential energy 2. drawn bow has potential energy a) needs a target to release b) energy mobilized only to the degree necessary c) results in appropriate behavior for achieving that goal; in other words the behavior is selected by the incentive II. THE HYPOTHALAMUS, HOMEOSTASIS, AND MOTIVATED BEHAVIOR A. Hypothalamus regulates 1. body temperature 2. fluid balance 3. energy balance B. Process (see overhead on hypothalamic regulation of homeostasis) 1. sensory transduction wherein a specialized neuron detects a deviation from homeostasis 2. response (insert figure showing the three categories of responses a) humoral b) ANS c) Somatic (motivated behavior) mediated through the lateral III. THE LONG TERM REGULATION OF FEEDING BEHAVIOR A. Energy balance 1. anabolism (part a of the figure shows anabolism during the prandial state when the blood is filled with nutrients) 2. catabolism (part b of the figure shows catabolism during the postabsorptive state when we are not eating) a) obesity results from excess intake in comparison to expenditure b) starvation results when expenditure exceeds intake c) constant weight results when the average of intake and expenditure are the same 3. regulation of energy balance based on a) energy reserves b) rate of replenishment B. Hormonal and hypothalamic regulation of body fat and feeding 1. homeostatic regulation of feeding behavior is mostly regulated by the thalamus detecting a drop in the level of a hormone released by fat cells (leptin) 2. body fat and food consumption a) lipostatic hypothesis: body tries to maintain consistent level of fat

2 Motivation 2 of 6 b) seen in the difficulty of losing or gaining weight c) thought to have a blood hormone related to fat levels; this was confirmed by parabiosis of obese and normal mice (1) the ob/ob mouse s weight moved toward normal (2) Friedman later isolated leptin and it was shown that leptin injections can reverse the obesity in ob/ob mice 3. the and feeding a) Hetherington and Ranson (1) showed that bilateral destruction of the lateral led to anorexia hypothalamic syndrome (a) lateral viewed as feeding center (2) ventromedial hypothalamic damage leads to obesity ventromedial hypothalamic syndrome (a) ventromedial viewed as satiety center (3) more research research shows that the syndromes have more to do with leptin signaling 4. the effects of elevated leptin levels on the (see overhead on increased leptin) a) elevated leptin detected by the αmsh & Cart neurons in the arcuate nucleus of the b) signals sent to (1) lateral which decreases eating behavior (2) paraventricular nucleus (a) to ANS where sympathetic activity is raised (b) anterior pituitary via hypophysiotropic hormones (i) secretion of TSH which increases metabolism (ii) secretion of ACTH which increases metabolism c) injections of αmsh & Cart mimic elevated leptin d) blocking αmsh & Cart increases feeding 5. the effects of decreased leptin levels on the (see overhead on decreased leptin)

3 Motivation 3 of 6 a) decreased leptin detected by the NPY & AgRP neurons in the arcuate nucleus of the b) signals sent to (1) lateral which increases eating behavior (2) paraventricular nucleus (a) to ANS where parasympathetic activity is raised (b) anterior pituitary (i) TSH secretion decreased (ii) ACTH secretion decreased c) The effects of lept in on the lateral 6. The control of feeding by the lateral a) Lesions of the lateral lead to reduced feeding b) Electrical stimulation of the lateral leads to increased eating. c) Stimulation or destruction also affects axons passing through this area d) Both the neurons in the lateral and the axons passing through it are important to the motivation of feeding behavior. (1) MCH (a) MCH neurons in lateral are connected to the arcuate nucleus (b) MCH neurons project, monosynpatically, throughout the cortex (c) Cortex is involved in the organization of goal-directed behaviors (d) Injection of MCH stimulates feeding (e) Mice without MCH show reduced feeding (2) Orexin (a) Orexin neurons found in the lateral (b) Orexin stimulates feeding when leptin levels fall (c) When leptin levels fall, both MCH and orexin increase IV. THE SHORT-TERM REGULATION OF FEEDING BEHAVIOR A. motivation to eat depends upon 1. how long it has been since we last ate 2. how much we ate then B. motivation to continue eating depends upon 1. how much we ve already eaten 2. what type of food we ve eaten C. Eating, Digestion, and Satiety

4 Motivation 4 of 6 1. three phases of eating a) cephalic response b) gastric phase c) substrate phase 2. three types of satiety signals a) gastric distension (1) vagus nerve sends signals from mechanosensory receptors in the stomach to the nucleus of the solitary tract (2) taste buds also send signals to the nucleus of the solitary tract (3) nucleus of the solitary tract sends signals to (a) ANS (b) Areas that inhibit feeding b) CCK (1) Released by stimulation of the intestines by certain foods, especially fatty foods (2) Affects vagal sensory axons (3) Has a synergistic effect with distension gastric

5 Motivation 5 of 6 c) Insulin (see the overhead on insulin) (1) Pancreatic β cells release insulin (2) Insulin transports glucose from bloodstream into nonneuronal cells (3) Insulin is required for anabolism (storage in liver, muscle, & fat cells) (4) Insulin is also required for catabolism (liberation from storage cells) (5) An increase in insulin results in lowered blood glucose levels (6) A decrease in insulin results in increased blood glucose levels V. WHY DO WE EAT? A. Intro 1. hedonic qualities 2. drive reduction 3. these are analogous to liking and wanting B. The role of Dopamine in Motivation 1. electrical stimulation of the lateral a) activates orexigenic neurons b) activates the DA mesocorticolimbic system (motivated behavior through reward) (1) destruction of these DA neurons leads to a decrease in eating 2. thought that the ventromedial tegmental area provided hedonic reward but no longer think that because a) destruction of pathways doesn t reduce liking but seems to reduce wanting b) stimulation of the DA neurons of the lateral produces wanting without changes in liking 3. we ll examine this system more in chapter 21 C. Serotonin, Food, and Mood 1. serotonin involved in the control of mood a) carbohydrates elevate mood 2. serotonin suppresses appetite 3. depression is comorbid with eating disorders probably due to 5-HT VI. OTHER MOTIVATED BEHAVIORS A. Intro 1. Like other systems studied they operate off the same principles a) Transduction of physiological stimuli in the blood to specialized regions of the b) Humoral and visceral responses initiated by the periventricular and medial c) Behavior mediated by the lateral B. Drinking

6 Motivation 6 of 6 1. Two different signals that lead to drinking a) Hypovolume (1) Volumetric thirst results from release of vasopressin (ADH) [we covered this in the last chapter] (2) pathways of volumetric thirst b) Hypertonicity (1) Osmotic thirst (a) Hypertonicity detected by OVLT (b) H 2 O pulled out of cells by osmotic pressure (c) Leads to changes in OVLT action potentials (d) OVLT connected to magnocellular cells C. Temperature Regulation (see overhead on temperature regulation) 1. temperature sensing neurons throughout the brain and spinal cord a) most important detectors in the anterior b) connections and effects