ACTH and corticosterone secretion following insulin in intact and in variously hypothalamic deafferented male rats

Adult male rats, intact (N) or with posterior (PHD), anterior (AHD) or complete (CHD) hypothalamic deafferentations, were injected with either 0.04 or 0.2 mu/100 g b.wt. of insulin. Forty-five minutes later they were decapitated and trunk blood was collected for serum glucose, adrenocorticotropic hormone (ACTH) and corticosterone (CS) determinations. The high insulin dose reduced serum glucose by approximately 50% and elicited a marked increase in serum ACTH and CS levels in all groups of animals as compared to the vehicle-treated group. In contrast, the low insulin dose which reduced serum glucose approximately 30% elicited a significant adrenocortical response only in the intact or PHD groups but failed to stimulate this response in animals with CHD or AHD. These results demonstrate that (1) CNS sites, outside the medial basal hypothalamus (MBH), mediate the adrenocortical response during the initial stages of hypoglycemia by a neural pathway impinging upon the CRF neurons from the rostral direction, and (2) the adrenocortical response during the more enhanced hypoglycemia stages is mediated by a systemic mechanism which acts directly on the MBH.