Cannabinoid agonist antagonizes cFos induced by intraperitoneal cholecystokinin

• Published in: Appetite 2007-07, Vol.49 (1), p.288-288
• Main Authors: Edwards, G.L., Gaddam, D.R., Freeman, K.G.
• Format: Article
• Language: English
• ISSN: 0195-6663; 1095-8304
• DOI: 10.1016/j.appet.2007.03.062

Cannabinoid agonist is reported to increase intake of highly palatable foods when injected into the fourth cerebroventricle [(2004). Physiological Behavior, 80, 611]. One possible mechanism for enhanced intake by cannabinoid agonists is attenuation of visceral signals from the gut. Our initial attempts to address this question have focused on induction of cFos by intraperitoneal cholecystokinin (CCK). It is well recognized the CCK induces cFos immunoreactivity in neurons of the caudal nucleus of the solitary tract (NTS) and area postrema (AP). We hypothesized that cannabinoid agonist will attenuate CCK-induced cFos in the hindbrain. We found that CCK induced a significant increase in cFos-immunoreactive neurons in the NTS and AP. The number of cFos-immunoreactive neurons was decreased significantly by prior application of the cannabinoid agonist CP55940. This reduction in cFos-immunoreactive neurons by CP 55940 was blocked by the CB1 receptor antagonist SR141716. Moreover, treatment with cannabinoid antagonist alone does not appear to significantly elevate cFos in the NTS. These observations suggest that cannabinoids may work in the NTS to blunt inhibitory signals from the gut resulting in elevated food intake. (Supported by the Department of Physiology & Pharmocology, University of Georgia).