| Abstract: | In this study we examined whether circulating glucocorticoids (GC) have a permissive facilitatory role in the hypothalamo–pituitary–adrenal (HPA) axis responses to neural or metabolic stimuli. In control sham operated rats the exposure to photic or acoustic neural stimuli and to either cytoglucopenia induced by 2-deoxyglucose (2-DG) or to hypoglycemia induced by insulin caused a significant 5-fold increase in serum ACTH as compared to basal non-stress levels. In adrenalectomized (Adex) rats tested under basal conditions at 4, 7 and 14 days post-Adex, serum ACTH gradually increased in a time-dependent manner, Also, at 4 days post-Adex the median eminence (ME) content of CRH-41 was markedly depleted but gradually recovered to control levels at 7 and 14 days post-Adex. The serum ACTH responses to both photic and acoustic stimuli tested at the same time points were completely inhibited. In contrast, administration of either insulin or 2-DG caused a marked increase in serum ACTH levels. In Adex rats, implanted with low corticosterone (CS) pellets which produced basal serum levels of CS, ME CRH-41 levels and serum ACTH were similar to control sham operated animals. Exposure to both neural stimuli resulted in a significant depletion in CRH-41 ME content and in a rise in serum ACTH as in the respective controls. On the other hand in rats implanted with high CS pellets which produced stress typical CS serum levels, the ME CRH-41 and serum ACTH responses to both stimuli were markedly inhibited. These results suggest that (1) the HPA axis responses to neural stimuli but not to metabolic stimuli require the presence of circulating GC (2), the lack of ACTH response to neural stimuli in Adex rats may not be related to the low CRH-41 ME content. |
