Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Sexually dimorphic nucleus wikipedia , lookup
Hypothyroidism wikipedia , lookup
Hormone replacement therapy (male-to-female) wikipedia , lookup
Graves' disease wikipedia , lookup
Hyperthyroidism wikipedia , lookup
Pituitary apoplexy wikipedia , lookup
Growth hormone therapy wikipedia , lookup
BIO 132 Neurophysiology Lecture 35 Motivation 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. Motivation Motivation – the driving force behind behavior Get food Sit in class Urinate Listen to music Sit in class Current Goal Behavior Motivations 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. 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). 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. 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) Energy Balance Caloric intake = caloric expenditure Normal weight Caloric intake > caloric expenditure Gain weight Caloric intake < caloric expenditure Lose weight Lipostatic Hypothesis First proposed in 1953, the lipostatic hypothesis states that the brain monitors fat levels and maintains them at some fixed setpoint amount. The lipostatic hypothesis requires that the fat communicate with the brain in some way. First suspected was some blood-borne chemincal (a hormone). 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) 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 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). Obese (ob/ob) Normal 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. 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. 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. Effects of Leptin nutrients Lateral zone Satiety Fat ventrical inhibit Periventricular zone Hunger leptin Feeding behavior Pituitary αMSH CART TRH CRH Arcuate nucleus TSH ACTH Caloric intake SNS thyroid hormone Metabolic rate cortisol