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
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
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DOI：
10.1159/000124652
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发表时间：
1986-01-01
影响因子：
4.1
通讯作者：
BARDEN, N
中科院分区：
文献类型：
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作者：
BEAULIEU, S;DIPAOLO, T;BARDEN, N
评估了大鼠杏仁中央核（ACE）在响应固定应激而控制 ACTH 分泌中的可能意义。应激和/或双侧 ACE 损伤时的 ACTH 分泌与特定下丘脑和杏仁核中的血清素能活性相关。 ACE 的双侧损伤导致血浆 ACTH 水平显着降低，以应对压力。然而，在上午 7 点至 11 点之间测量的基础血浆 ACTH 水平在对照组和病变组中是相同的。对完整动物施加压力不会改变以下任何区域的血清素能活性：下丘脑室旁核（PVH）、腹内侧核（VMH）和背内侧核（DMH）；下丘脑前区（AHA）；杏仁核的外侧部分（ABL）、内侧杏仁核（AME）和皮质核（ACO）。然而，ACE 的损伤增加了除 VMH 之外的所有这些结构中的血清素能活性。对病变动物施加固定应激，可将 PVH、AHA 和 DMH 中的血清素能活性降低至控制水平，并将 VMH 中的活性降低至对照水平以下。在杏仁核富含糖皮质激素受体的区域，即 AME、ACO 和 ABL 核中，血清素能活性保持在增加的水平。这些结果为杏仁核中央核在控制 ACTH 分泌中的刺激作用提供了证据。此外，他们证实了杏仁核复合物通过与血清素能系统相互作用来控制糖皮质激素对 ACTH 分泌的延迟负反馈的影响。
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 serotonergic 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 ocntrol 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. The 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.