Схема. Action of Satiety Signals on Hypothalamic Neurons Involved in Control of Hunger and Satiety. Перевести на русский язык = Translate into Russian Модификация: Модификация: Carlson N.R. Physiology of Behavior. Pearson, 11th ed., 2013, 771 p., См.: Физиология человека: Литература. Иллюстрации.       Примечание: The brain stem contains neural circuits that are able to control acceptance or rejection of sweet or bitter foods and can even be modulated by satiation or physiological hunger signals, such as a decrease in glucose metabolism or the presence of food in the digestive system. The area postrema and nucleus of the solitary tract (AP/NST) receive signals from the tongue, stomach, small intestine, and liver and send. the information on to many regions of the forebrain. These signals interact and help to control food intake. Lesions of the AP/NST disrupt both glucoprivic and lipoprivic eating. The lateral hypothalamus contains two sets of neurons whose activity increases eating and decreases metabolic rate. These neurons secrete the peptides orexin and MCH (melanin-concentrating hormone). Food deprivation increases the level of these peptides, and mice with a targeted mutation against MCH undereat. Secretion of orexin also keeps animals from sleeping through the time for a meal if food is available only intermittently. The axons of these neurons project to regions of the brain involved in motivation, movement, and metabolism. The release of neuropeptide Y in the lateral hypothalamus induces ravenous eating, an effect that is produced by excitatory connections of NPYsecreting neurons with the orexin and MCH neurons. NPY neurons in the arcuate nucleus of the hypothalamus receive input from glucose-sensitive neurons in the medulla. NPY neurons are the primary target of ghrelin in the hypothalamus. Ghrelin also activates the mesolimbic reinforcement system by stimulating dopaminergic neurons in the ventral tegmental area, which increases the release of DA in the nucleus accumbens. When NPY is infused in the paraventricular nucleus, it decreases metabolic rate. Levels of NPY increase when an animal is deprived of food and fall again when the animal eats. A drug that blocks NPY receptors suppresses eating. NPY neurons also release a peptide called AGRP. This peptide serves as an antagonist at MC4 receptors and, like NPY, stimulates eating. Endocannabinoids, whose action is mimicked by THC, the active ingredient in marijuana, also stimulate eating, apparently by increasing the release of MCH and orexin. Leptin, the long-term satiety hormone secreted by well-stocked adipose tissue, desensitizes the brain to hunger signals. It binds with receptors in the arcuate nucleus of the hypothalamus, where it inhibits NPY-secreting neurons, increasing metabolic rate and suppressing eating. However, low levels of leptin, which indicate a loss of fat tissue, provide a hunger signal more potent than high levels of leptin, which indicate a gain of fat tissue. The arcuate nucleus also contains neurons that secrete CART (cocaine- and amphetamine-regulated transcript), a peptide that suppresses eating. These neurons, which are activated by leptin, have inhibitory connections with MCH and orexin neurons in the lateral hypothalamus. CART neurons also secrete a peptide called рў-MSH, which serves as an agonist at MC4 receptors and inhibits eating. Ghrelin, which activates NPY/AGRP neurons and stimulates hunger, also inhibits CART/рў-MSH neurons and suppresses the satiating effect of the peptides secreted by these neurons. The anorexigenic peptide, PYY, which is released by the gastrointestinal system, suppresses the release of NPY and AGRP. p. 418