Chapter 10 Internal Regulation

Temperature Regulation Temperature affects many aspects of behavior. Temperature regulation is vital to the normal functioning of many behavioral processes. Homeostasis refers to temperature regulation and other biological processes that keep certain body variables within a fixed range.

Temperature Regulation A set point refers to a single value that the body works to maintain. –Examples: Levels of water, oxygen, glucose, sodium chloride, protein, fat and acidity in the body. Processes that reduce discrepancies from the set point are known as negative feedback. Allostasis refers to the adaptive way in which the body changes its set point in response to changes in life or the environment.

Temperature Regulation Temperature regulation is one of the body’s biological priorities. –Uses about two-thirds of our energy/ kilocalories per day. Basal metabolism is the energy used to maintain a constant body temperature while at rest.

Temperature Regulation Poikilothermic refers to the idea that the body temperature matches that of the environment. – Amphibians, reptiles and most fish. The organism lacks the internal, physiological mechanisms of temperature regulation. Temperature regulation is accomplished via choosing locations in the environment.

Temperature Regulation Homeothermic refers to the use of internal physiological mechanisms to maintain an almost constant body temperature. –Characteristic of mammals and birds. Requires energy and fuel. Sweating and panting decrease temperature. Increasing temperature is accomplished via shivering, increasing metabolic rate, decreasing blood flow to the skin, etc.

Temperature Regulation Mammals evolved to have a constant temperature of 37˚ C (98˚ F). –Muscle activity benefits from being as warm as possible and ready for vigorous activity. –Proteins in the body break their bonds and lose their useful properties at higher temperatures. –Reproductive cells require cooler temperatures.

Temperature Regulation Body temperature regulation is predominantly dependent upon areas in the preoptic area/ anterior hypothalamus (POA/AH). The POA/AH partially monitors the body’s temperature by monitoring its own temperature. –Heating the POA/AH leads to panting or shivering; cooling leads to shivering. Cells of the POA/AH also receive input from temperature sensitive receptors in the skin.

Fig. 10-5, p. 300

Temperature Regulation Bacterial and viral infections can cause a fever, part of the body’s defense against illness. Bacteria and viruses trigger the release of leukocytes which release small proteins called cytokines. Cytokines attack intruders but also stimulate the vagus nerve.

Temperature Regulation (Continued) The vagus nerve stimulates the hypothalamus to initiate a fever. Some bacteria grow less vigorously in warmer than normal body temperature. However, a fever of above 39˚ C (103˚ F) does the body more harm than good.

Thirst Water constitutes 70% of the mammalian body. Water in the body must be regulated within narrow limits. The concentrations of chemicals in water determines the rate of all chemical reactions in the body.

Thirst Mechanisms of water regulation vary for humans. Water can be conserved by: –Excreting concentrated urine. –Decreasing sweat and other autonomic responses. Most often water regulation is accomplished via drinking more water than we need and excreting the rest.

Thirst Vasopressin is a hormone released by the posterior pituitary which raises blood pressure by constricting blood vessels. –helps to compensate for the decreased water volume. Vasopressin is also known as an antidiuretic hormone because it enables the kidneys to reabsorb water and excrete highly concentrated urine.

Thirst Two different kinds of thirst include: 1.Osmotic thirst – a thirst resulting from eating salty foods. 2.Hypovolemic thirst – a thirst resulting from loss of fluids due to bleeding or sweating. Each kind of thirst motivates different kinds of behaviors.

Thirst Osmotic thirst occurs because the human body maintains a combined concentration of solutes at a fixed level of.15 M (molar). Solutes inside and outside a cell produce osmotic pressure, the tendency of water to flow across a semi-permeable membrane from an area of low solute concentration to an area of high solute concentration. –Occurs when solutes are more concentrated on one side of the membrane.

Fig. 10-6, p. 304

Thirst Eating salty food causes sodium ions to spread through the blood and extracellular fluid of the cell. The higher concentration of solutes outside the cell results in osmotic pressure, drawing water from the cell to the extracellular fluid. Certain neurons detect the loss of water and trigger osmotic thirst to help restore the body to the normal state.

Thirst The brain detects osmotic pressure from: –Receptors around the third ventricle. –The OVLT (organum vasculosum laminae terminalis) and the subfornical organ (detect osmotic pressure and salt content). –Receptors in the periphery, including the stomach, which detect high levels of sodium.

Thirst Receptors in the OVLT, subfornical organ, stomach and elsewhere relay information to areas of the hypothalamus including: – the supraoptic nucleus – paraventricular nucleus. Both control the rate at which the posterior pituitary releases vasopressin. Receptors also relay information to the lateral preoptic area which controls drinking.

Fig. 10-7, p. 304

Thirst When osmotic thirst is triggered, water that you drink has to be absorbed through the digestive system. To inhibit thirst, the body monitors swallowing and detects the water contents of the stomach and intestines.

Thirst Hypovolemic thirst is thirst associated with low volume of body fluids. –Triggered by the release of the hormones vasopressin and angiotensin II, which constrict blood vessels to compensate for a drop in blood pressure. Angiotensin II stimulates neurons in areas adjoining the third ventricle. Neurons in the third ventricle send axons to the hypothalamus where angiotensin II is also released as a neurotransmitter.

Fig. 10-8, p. 305

Thirst Animals with osmotic thirst have a preference for pure water. Animals with hypovolemic thirst have a preference for slightly salty water as pure water dilutes body fluids and changes osmotic pressure. Sodium-specific hunger, a strong craving for salty foods. – develops automatically to restore solute levels in the blood.

Table 10-1, p. 305

Hunger Animals vary in their strategies of eating, but humans tend to eat more than they need at the given moment. A combination of learned and unlearned factors contribute to hunger.

Hunger The function of the digestive system is to break down food into smaller molecules that the cells can use. Digestion begins in the mouth where enzymes in the saliva break down carbohydrates. Hydrochloric acid and enzymes in the stomach digest proteins.

Fig , p. 308

Hunger The small intestine has enzymes that digest proteins, fats, and carbohydrates and absorbs digested food into the bloodstream. The large intestine absorbs water and minerals and lubricates the remaining materials to pass as feces.

Hunger At the age of weaning, most mammals lose the intestinal enzyme lactase, which is necessary for metabolizing lactose. Lactose is the sugar found in milk. Milk consumption after weaning can cause gas and stomach cramps. Declining levels of lactase may be an evolutionary mechanism to encourage weaning.

Hunger Most human adults have enough lactase to consume milk and other dairy products throughout the lifetime. Nearly all people in China and surrounding countries lack the gene that enables adults to metabolize lactose. –Only small quantities of dairy products can be consumed.

Fig , p. 309

Hunger A carnivore is an animal that eats meat and necessary vitamins are found in the meat consumed. Herbivores are animals that exclusively eat plants. Omnivores are animals that eat both meat and plants.

Hunger Herbivores and omnivores must distinguish between edible and inedible substances to find sufficient vitamins and minerals. Selecting foods to eat is usually accomplished via imitation of others.

Hunger Other strategies of selecting food include: –Selecting sweet foods and avoiding bitter foods. –Preferring things that taste familiar. –Learning from consequences that happen after a food is consumed. A conditioned taste aversion is a distaste for food that develops if the food makes one ill.

Hunger The brain regulates eating through messages from the mouth, stomach, intestines, fat cells and elsewhere. The desire to taste and other mouth sensations, such as chewing, are also motivating factors in hunger and satiety. Sham feeding experiments, in which everything an animals eats leaks out of a tube connected to the stomach or esophagus, do not produce satiety.

Hunger The main signal to stop eating is the distention of the stomach. The vagus nerve conveys information about the stretching of the stomach walls to the brain. The splanchnic nerves convey information about the nutrient contents of the stomach.

Hunger The duodenum is the part of the small intestine where the initial absorption of significant amounts of nutrients occurs. Distention of the duodenum can also produce feelings of satiety. The duodenum also releases the hormone cholecystokinin (CCK), which helps to regulate hunger.

Hunger Cholecystokinin (CCK) released by the duodenum regulates hunger by: –Closing the sphincter muscle between the stomach and duodenum and causing the stomach to hold its contents and fill faster. –Stimulating the vagus nerve to send a message to the hypothalamus that releases a chemical similar to CCK.

Hunger Glucose, insulin, and glucagon levels also influence feelings of hunger. Most digested food enters the bloodstream as glucose, an important source of energy for the body and nearly the only fuel used by the brain. When glucose levels are high, liver cells convert some of the excess into glycogen and fat cells convert it into fat. When low, liver converts glycogen back into glucose.

Hunger Insulin is a pancreatic hormone that enables glucose to enter the cell. Insulin levels rise as someone is getting ready for a meal and after a meal. In preparation for the rush of additional glucose about to enter the blood, high insulin levels let some of the existing glucose in the blood to enter the cells. Consequently, high levels of insulin generally decrease appetite.

Fig , p. 311

Hunger Glucagon is also a hormone released by the pancreas when glucose levels fall. Glucagon stimulates the liver to convert some of its stored glycogen to glucose to replenish low supplies in the blood. As insulin levels drop, glucose enters the cell more slowly and hunger increases.

Hunger If insulin levels constantly stay high, the body continues rapidly moving blood glucose into the cells long after a meal. –Blood glucose drops and hunger increases in spite of the high insulin levels. –Food is rapidly deposited as fat and glycogen. –The organism gains weight.

Fig , p. 311

Hunger In people with diabetes, insulin levels remain constantly low, but blood glucose levels are high. –People eat more food than normal, but excrete the glucose unused and lose weight.

Fig , p. 311

Hunger Long-term hunger regulation is accomplished via the monitoring of fat supplies by the body. The body’s fat cells produce the peptide leptin, which signals the brain to increase or decrease eating. Low levels of leptin increase hunger.

Hunger High levels of leptin do not necessarily decrease hunger. –Most people are obese because they are less sensitive to leptin. –Some people are obese because of a genetic inability to produce leptin.

Hunger Information from all parts of the body regarding hunger impinge into two kinds of cells in the arcuate nucleus. The arcuate nucleus is a part of the hypothalamus containing two sets of neurons: 1. neurons sensitive to hunger signals. 2. neurons sensitive to satiety signals.

Hunger Neurons of the arcuate nucleus specifically sensitive to hunger signals receive input from: –The taste pathways. –Axons releasing the neurotransmitter ghrelin. Ghrelin is released as a neurotransmitter in the brain and also in the stomach to trigger stomach contractions.

Hunger Input to the satiety-sensitive cells of the arcuate nucleus include signals of both long- term and short-term satiety: –Distention of the intestine triggers neurons to release the neurotransmitter CCK. –Blood glucose and body fat increase blood levels of the hormone insulin. –Some neurons release a smaller peptide related to insulin as a transmitter. –Leptin provides additional input.

Hunger Output from the arcuate nucleus goes to the paraventricular nucleus of the hypothalamus. The paraventricular nucleus is a part of the hypothalamus that inhibits the lateral hypothalamus which is important for feelings of hunger and satiety. Axons from the satiety-sensitive cells of the arcuate nucleus deliver an excitatory message to the paraventricular nucleus which triggers satiety.

Hunger Input from the hunger-sensitive neurons of the arcuate nucleus is inhibitory to both the paraventricular nucleus and the satiety- sensitive cells of the arcuate nucleus itself. –inhibitory transmitters include GABA, neuropeptide Y (NPY), and agouti-related peptide (AgRP). Neuropeptide Y (NPY) and agouti-related peptide (AgRP) are inhibitory transmitters that block the satiety action of the paraventricular nucleus and provoke overeating.

Hunger Output from the paraventricular nucleus acts on the lateral hypothalamus. –The lateral hypothalamus controls insulin secretion and alters taste responsiveness. Animals with damage to this area refuse food and water and may starve to death unless force fed.

Fig , p. 315

Hunger The lateral hypothalamus contributes to feeding by: –Detecting hunger and sending messages to make food taste better. –Arousing the cerebral cortex to facilitate ingestion, swallowing, and to increase responsiveness to taste, smell and sights of food. –Increasing the pituitary gland’s secretion of hormones that increase insulin secretion. –Increasing digestive secretions.

Fig , p. 316

Hunger Damage to the ventromedial hypothalamus that extends to areas outside can lead to overeating and weight gain. Those with damage to this area eat normal sized but unusually frequent meals. Increased stomach secretions and motility causes the stomach to empty faster than usual. Damage increases insulin production and much of the meal is stored as fat.

Fig b, p. 316

Table 10-2, p. 317

Hunger People with a mutated gene for the receptors melanocortin overeat and become obese. –Melanocortin is a neuropeptide responsible for hunger. Prader-Willis syndrome is a genetic condition marked by mental retardation, short stature, and obesity. –Blood levels of the peptide ghrelin is five times higher than normal.

Hunger Although a single gene can not be identified, a genetic influence has been established in many factors contributing to obesity. Monozygotic twins resemble each other more the dizygotic twins in factors contributing to obesity. –Examples: how much stomach distention influences the ending of eating, how much one overeats when food tastes good.

Hunger Obesity can also be a function of genes interacting with changes in the environment. –Example: Diet changes of Native American Pimas of Arizona and Mexico. Obesity has become common in the United States and has increased sharply since the 1970’s. –Attributed to life-style changes, increased fast-food restaurants, increased portion sizes, and high use of fructose in foods.

Hunger Weight-loss is often difficult and specialist rarely agree. Plans should include increased exercise and decreased eating. Some appetite-suppressant drugs such as fenfluramine and phentermine block reuptake of certain neurotransmitters to produce brain effects similar to that of a completed meal. “Orlistat” is drug that prevents the intestines from absorbing fats.

Hunger Anorexia nervosa is an eating disorder associated with an unwillingness to eat as much as needed. Genetic predisposition is likely. –no clear link has been established Associated with a fear of becoming fat and not a disinterest in food. Biochemical abnormalities in the brain and blood are probably not the cause, but a result of the weight loss.

Fig , p. 317

Hunger Bulimia nervosa is an eating disorder in which people alternate between extreme dieting and binges of overeating. –Some force vomiting after eating. Associated with decreased release of CCK, increased release of ghrelin, and alterations of several other hormones and transmitters. –May be the result and not the cause of the disorder. –Reinforcement areas of the brain also implicated.