PATHWAYS OF FOS EXPRESSION IN LOCUS-CERULEUS, DORSAL VAGAL COMPLEX, AND PVN IN RESPONSE TO INTESTINAL LIPID

Exogenous cholecystokinin (CCK) injected peripherally mimics effects o f lipid entering the intestine on food intake and gastric motility via vagal afferents and induces c-fos expression in the locus ceruleus co mplex (LCC), nucleus of the solitary tract (NTS), area postrema (AP), and paraventricular nucleus (PVN). However, the role of peripheral end ogenous CCK in induction of c-fos expression in the brain at ingestion of nutrients is controversial. In awake rats, intraduodenal lipid inf usion markedly increased Fos protein-like immunoreactivity (FLI) in th ese brain nuclei. Perivagal capsaicin pretreatment reduced the increas e of FLI in the LCC, NTS, and PVN by 66-86% and in the AP by 46%. The CCK-A receptor antagonist MK-329 (0.1 mg/kg ip) diminished the FLI inc rease in LC, NTS,AP, and PVN by 39-100%; the CCK-B receptor antagonist L-365,260 reduced the increased FLI in the AP by 54%. After capsaicin pretreatment, both CCK antagonists had additional inhibitory effects only on FLI in the AP. These findings suggest that entry of lipid into the intestine activates c-fos in the LCC, NTS, and PVN predominantly via CCK-A receptors on vagal afferents and in the AP via vagal and non vagal pathways, as well as CCK-B and CCK-A receptors.