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Understanding Neurophysiology of Motivation: Hunger, Thirst, and Temperature Regulation

This lecture explores the underlying mechanisms affecting rudimentary motivations such as hunger, thirst, and warmth. It also looks at the common elements behind the feedback loops controlling these motivations. Topics include homeostatic feedback loops, long-term feeding behavior, the lipostatic hypothesis, and the role of leptin in regulating metabolism and appetite.

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Understanding Neurophysiology of Motivation: Hunger, Thirst, and Temperature Regulation

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  1. BIO 132 Lecture 35 Motivation Neurophysiology

  2. Lecture Goals: • Understanding the underlying mechanisms affecting rudimentary motivations (hunger, thirst, warmth, etc). • Appreciating the common elements behind the feedback loops controlling hunger, thirst, and temperature regulation.

  3. Get food Sit in class Urinate Listen to music Motivation • Motivation – the driving force behind behavior • The brain area(s) responsible for keeping track and deciding on what the current behavior should be is still unknown. • Many motivations arise from internal homeostatic feedback loops. Current Goal Sit in class Behavior Motivations

  4. Hunger • Hunger: the motivation to eat • Hunger is affected by more than one homeostatic feedback loop. • Maintenance of blood glucose levels (short-term feeding behavior) • Maintenance of fat stores (long-term feeding behavior) • Hunger can also be affected by things other than homeostatic feedback loops such as mood (bored, sad, happy, anxious, etc).

  5. Long-term Feeding Behavior • Goal of long-term feeding behavior: Maintain long-term energy stores (fat). • Fat has twice the energy (per weight) as glucose and doesn’t require excess water storage like glucose (fat isn’t osmotically active). • The body has a set-point for the amount of fat it would like stored on the body.

  6. Maintenance of Fat Stores • Experimentally, rats were given food to eat whenever they wanted (ad libitum), but at two time periods of the experiment were deprived of food and forced fed. fasted force-fed Body weight (g) set-point Time (days)

  7. Energy Balance • Caloric intake = caloric expenditure Normal weight • Caloric intake > caloric expenditure Gain weight • Caloric intake < caloric expenditure Lose weight

  8. Lipostatic Hypothesis • First proposed in 1953, the lipostatic hypothesis states that the brain monitors fat levels and maintains them at some fixed set-point amount. • The lipostatic hypothesis requires that the fat communicate with the brain in some way. • First suspected was some blood-borne chemincal (a hormone).

  9. Hormone from Fat • Evidence of a hormone from the fat (1960s): • Parabiosis (the fusing of two animals so that they share the same blood) of a genetically obese mouse to a normal mouse caused the obese mouse to become thin (normal weight). Obese Normal Surgically fused (share blood)

  10. Hormone from Fat • It was apparent that the blood carried some signal to the brain from the fat that allowed the brain to monitor the levels of fat. • The hormone went undiscovered until 1994. • The gene that made genetically obese mice (ob/ob) was finally isolated and its product synethesized. • The product of the gene was named leptin

  11. Hormone from Fat - Leptin • Once isolated an synthesized, leptin could be injected into obese mice (ob/ob) that cannone make leptin themselves, and the mice would become thin (normal weight). Normal Obese (ob/ob) leptin

  12. How Does Leptin Work? • It was known since the 1940s that destruction of the hypothalamus led to abnormal food intake. • Leptin was theorized to have its effect on the hypothalamus. • It is now known that leptin binds to αMSH and CART receptors in the arcuate nucleus of the hypthalamus. • αMSH stands for alpha-melanocyte-stimulating hormone. • CART stands for cocaine-and amphetamine-regulated transcript. * You do not need to memorize these names, just the abbreviations.

  13. Effects of Leptin on the Arcuate Nucleus • Once leptin binds to receptors in the arcuate nucleus, activated neurons project to the periventricular and the lateral zones. • The periventricular zone activates both the sympathetic NS and neurons projecting to the pituitary gland. • Activated SNS causes in increase in metabolism (burning calories). • Hypothalamic neurons projecting to the pituitary release thyroid releasing hormone (TRH) which causes the release of thyroid stimulating hormone (TSH) from secretory cells in the anterior pituitary, causing the release of thyroid hormone from the thyroid gland, increasing metabolism.

  14. Effects of Leptin on the Arcuate Nucleus • Other hypothalamic neurons projecting to the pituitary release corticotropin releasing hormone (CRH) which causes the release of adrenocorticotropic hormone (ACTH) from secretory cells of the pituitary, causing the release of cortisol from the adrenal gland which increases metabolism. • The lateral zone activates neurons that decrease the motivation to eat by decreasing hunger and increasing the feeling of satiety. This decreases caloric intake.

  15. Satiety ventrical Hunger αMSH CART ACTH TRH CRH SNS TSH thyroid hormone cortisol Metabolic rate Effects of Leptin nutrients Periventricular zone Lateral zone inhibit Fat Feeding behavior leptin Pituitary Caloric intake Arcuate nucleus

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