The Ventral Pallidum as a Non-homeostatic Feeding Relay
In the wild, most animals consume food strictly for survival, and their feeding behaviors follow homeostatic mechanisms. Unlike most animals, humans, laboratory rats and pets engage in non-homeostatic as well as homeostatic feeding. Non-homeostatic feeding is postulated to lead to brain deregulation and disease (Berthoud, 2007; Neel, 1962; Ravussin and Bogardus, 2000; Speakman, 2008; Woods et al., 2004). In this dissertation, I propose that the VPm is a critical brain region that modulates non-homeostatic feeding. Glutamatergic manipulations of the VPm induce feeding in rats fed ad libitum and additionally, modulate activity in hypothalamic areas implicated in the regulation of feeding such as the LH, DMH and PVN. Moreover, these pharmacological manipulations of the VPm which induce feeding are independent of orexin/hypocretin and MCH expressing neurons in the LH. This lack of orexin/hypocretin and MCH involvement suggests that feeding induced in satiated rats by excitation of the VPm does not operate via the traditional hypothalamic mechanisms implicated in the regulation of homeostatic feeding. Furthermore, behavioral experiments indicate an additional difference between feeding induced by excitation of the VPm and homeostatic feeding such as fasting. GABAergic manipulations of the VPm induce a preferential increase of fat intake in rats fed ad libitum while 24-h food deprivation does not. These results also suggest that the VPm might have a role in the regulation of fat intake. Finally, my experiments suggest that GABAergic manipulations of the AcbSh can modulate LH activity independently of the integrity of the VPm.