Abstract
Classically, feeding is regulated by an alternation between "hunger" signals, which activate specific hunger centres in the hypothalamus, and "satiety signals", which include both circulating factors (such as plasma concentrations of leptin and insulin) and neurally-mediated signals from the gastro-intestinal tract. One important satiety signal is the brain-gut peptide cholecystokinin (CCK). Peripheral CCK acts on afferent nerve fibres of the gastric vagus nerve, these vagal neurons project to the caudal brainstem, where they activate neurons that project to hypothalamic nuclei involved in appetite regulation. In particular, peripheral injections of CCK activate neurons in the nucleus tractus solitarii and ventrolateral medulla, including specific subpopulations of the noradrenergic neurons of the A1 and A2 cell groups. We have shown that neurons in the nucleus tractus solitarii that express prolactin-releasing peptide (PrRP) are activated rapidly by food ingestion. Blockade of PrRP signalling increased food intake and attenuated CCK-induced anorexia. All these data suggest that PrRP is a central satiety signal that mediates the peripheral satiety signal, CCK. [J Physiol Sci. 2008;58 Suppl:S42]
