CHOLECYSTOKININ INDUCES FOS EXPRESSION IN CATECHOLAMINERGIC NEURONS OF THE MACAQUE MONKEY CAUDAL MEDULLA

Systemic administration of cholecystokinin octapeptide (CCK) slows gas tric emptying, inhibits feeding, and stimulates pituitary hormone rele ase 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 trea tment. Monkeys were injected intravenously with CCK (3 or 15 mu g/kg b .wt) or vehicle solution (0.15 M NaCl), then were anesthetized and per fused with fixative 75 min later. Coronal tissue sections through the caudal medulla were processed for immunocytochemical localization of t he immediate-early gene product Fos as a marker of stimulus-induced ne uronal 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 activate d to express Fos in monkeys after CCK treatment, similar to previous r eports in rats. Treatment-activated neurons included substantial propo rtions of the A1/C1 and A2/C2 catecholaminergic cell groups, whereas n eurons in the locus coeruleus (A6 cell group) were not activated. Thes e results indicate that the autonomic, behavioral, and neuroendocrine effects produced by systemic administration of CCK involve hindbrain n eural systems whose anatomical and chemical features are comparable in rats and primates. (C) 1997 Elsevier Science B.V.