Plasma hormone levels and central c-Fos expression in ferrets after systemic administration of cholecystokinin

Posterior pituitary hormone secretion and central neural expression of the immediate-early gene product c-Fos was examined in adult ferrets after intr avenous administration of CCK octapeptide. Pharmacological doses of CCK (1, 5, 10, or 50 mug/kg) did not induce emesis, but elicited behavioral signs of nausea and dose-related increases in plasma vasopressin (AVP) levels wit hout significant increases in plasma oxytocin (OT) levels. CCK activated ne uronal c-Fos expression in several brain stem viscerosensory regions, inclu ding a dose-related activation of neurons in the dorsal vagal complex (DVC) . Activated brain stem neurons included catecholaminergic and glucagon-like peptide-1-positive cells in the DVC and ventrolateral medulla. In the fore brain, activated neurons were prevalent in the paraventricular and supraopt ic nuclei of the hypothalamus and also were observed in the central nucleus of the amygdala and bed nucleus of the stria terminalis. Activated hypotha lamic neurons included cells that were immunoreactive for AVP, OT, and cort icotropin-releasing factor. Comparable patterns of brain stem and forebrain c-Fos activation were observed in ferrets after intraperitoneal injection of lithium chloride (LiCl; 86 mg/kg), a classic emetic agent. However, LiCl activated more neurons in the area postrema and fewer neurons in the nucle us of the solitary tract compared with CCK. Together with results from prev ious studies in rodents, our findings support the view that nauseogenic tre atments activate similar central neural circuits in emetic and nonemetic sp ecies, despite differences in treatment-induced emesis and pituitary hormon e secretion.