| pubmed-article:9372200 | pubmed:abstractText | Systemic administration of cholecystokinin octapeptide (CCK) slows gastric emptying, inhibits feeding, and stimulates pituitary hormone release in rats and primates. To characterize the central neural circuits that mediate these effects in primates, the present study analyzes the distribution and chemical phenotypes of caudal medullary neurons that are activated in rhesus and cynomolgus macaque monkeys after CCK treatment. Monkeys were injected intravenously with CCK (3 or 15 micrograms/kg b.wt) or vehicle solution (0.15 M NaCl), then were anesthetized and perfused with fixative 75 min later. Coronal tissue sections through the caudal medulla were processed for immunocytochemical localization of the immediate-early gene product Fos as a marker of stimulus-induced neuronal activation, and were double-labeled for tyrosine hydroxylase to identify catecholaminergic cells. Many neurons in the area postrema, nucleus of the solitary tract, and ventrolateral medulla were activated to express Fos in monkeys after CCK treatment, similar to previous reports in rats. Treatment-activated neurons included substantial proportions of the A1/C1 and A2/C2 catecholaminergic cell groups, whereas neurons in the locus coeruleus (A6 cell group) were not activated. These results indicate that the autonomic, behavioral, and neuroendocrine effects produced by systemic administration of CCK involve hindbrain neural systems whose anatomical and chemical features are comparable in rats and primates. | lld:pubmed |
