Control of ACTH secretion by the central nucleus of the amygdala: implication of the serotoninergic system and its relevance to the glucocorticoid delayed negative feedback mechanism

Abstract

The possible implication of the amygdaloid central nucleus (ACE) of the rat in the control of ACTH secretion in response to immobilization stress was assessed. The ACTH secretion, in response to stress and/or bilateral lesions of the ACE, was correlated with the serotoninergic activity in specific hypothalamic and amygdaloid nuclei. Bilateral lesions of the ACE produced a striking decrease of plasma ACTH levels in response to stress. However, basal plasma ACTH levels measured between 7 and 11 a.m. were identical in both control and lesioned groups. Stress, applied to intact animals, did not modify the serotoninergic activity in any of the following areas: hypothalamic paraventricular (PVH), ventromedial (VMH) and dorsomedial (DMH) nuclei; the anterior hypothalamic area (AHA); the lateral part of the basal amygdaloid nucleus (ABL), the amygdaloid medial (AME) and cortical (ACO) nuclei. However, lesion of the ACE increased the serotoninergic activity in all these structures except for the VMH. Immobilization stress applied to lesioned animals decreased the serotoninergic activity to control levels in the PVH, AHA and DMH and decreased the activity to below control levels in the VMH. The serotoninergic activity remained at an increased level in the glucocorticoid receptor-rich areas of the amygdala, namely the AME, ACO and ABL nuclei. These results provide evidence for a stimulatory role of the central nucleus of the amygdala in the control of ACTH secretion. Moreover, they substantiate an implication of the amygdaloid complex in the control of the delayed negative feedback of glucocorticoids on ACTH secretion via interaction with the serotoninergic system.