Paraventricular nucleus lesions abolish the inhibition of feeding induced by systemic cholecystokinin

Abstract

Peripherally administered cholecystokinin (CCK) initiates a behavioral syndrome which includes reduced food consumption and reduced exploratory behaviors. Previous studies suggest that CCK stimulates receptors in the gut, activating the vagus nerve, which relays sensory information to the nucleus tractus solitarius (NTS) and its ascending pathways [5, 6, 7, 41]. Terminal regions of ascending NTS projections include the paraventricular nucleus of the hypothalamus (PVN), the central nucleus of the amygdala (CNA), and the bed nucleus of the stria terminalis (BNST). Lesions of these three target sites were performed in rats to test the hypothesis that structures postsynaptic to the NTS mediate the behavioral syndrome induced by CCK. Knife cut lesions of the PVN abolished the reductions in feeding induced by CCK (5 and 10 μg/kg IP), as compared to sham lesioned control rats. PVN lesions only partially attenuated the reductions in exploration induced by CCK (2.5, 5, and 10 μg/kg IP), as compared to sham lesioned control rats. Electrolytic lesions of the CNA partially attenuated the reductions in exploratory behavior induced by CCK (2.5, 5, and 10 μg/kg IP), and had no effect on the reductions in feeding induced by CCK (5 and 10 μg/kg IP). Electrolytic lesions of the BNST had no effect on either the reductions in feeding or the reductions in exploration induced by CCK. The PVN appears to be one critical forebrain target site for mediating the actions of CCK on feeding. The CNA appears to facilitate the actions of CCK on exploration. Individual components of the behavioral syndrome induced by CCK may be mediated by anatomically distinct forebrain loci.