Metabolic hunger signals caused by glucoprivation or liproprivation arise from detectors in the liver and medulla; these signals activate the MCH and orexin neurons of the lateral hypothalamus through a system of neurons that secrete a neurotransmitter called neuropeptide Y (NPY), a potent stimulator of food intake Carlson 410. Infusion of NPY into the hypothalamus produces ravenous, almost frantic eating. Rats who receive an infusion of this peptide will work very hard, pressing many times a lever for each morsel of food; they will eat food made bitter with quinine, and they will continue to drink milk even when doing so means that they will receive an electric shock to the tongue (Flood and Morley, 1991).
NPY appears to have at lest two sites of action in the hypothalamus. When infused in the lateral hypothalamus, it produces eating. When infused in the paraventricular nucleus, located in the medial hypothalamus around the dorsal part of the third ventricle, it produced metabolic effects, including insulin secretion, and a decrease in body temperature (Currie and Coscina, 1996). These effects complement the increased appetite by preserving the body's energy supplies.
Levels of NPY are affected by hunger and satiety signals Sahu, Kalra and Kalra (1988) found that hypothalamic levels of NPY are increased by food deprivation and lowered by eating. In addition Myers et al. (1995) found that hypothalamic injections of a drug that blocks NPY receptors suppress eating caused by food deprivation. This last finding in particular, provides strong evidence that normal food intake is at least partially stimulated by NPY.
Neurons that secrete NPY are found in the arcuate nucleus, located in the hypothalamus at the base of the third ventricle. The nucleus also contains neurosecretory cells whose hormones control the secretions of the anterior pituitary gland. The NPY neurons send a projection of axons to the paraventricular nucleus, the region where infusions of NPY affect metabolic functions.