Response of the hypothalamo-pituitary-adrenal axis to nicotine
Response of the hypothalamo-pituitary-adrenal axis to nicotine
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DOI：
10.1016/s0306-4530(97)00079-6
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发表时间：
1998-02-01
影响因子：
3.7
通讯作者：
Sharp, BM
中科院分区：
文献类型：
--
作者：
Matta, SG;Fu, YT;Sharp, BM
尼古丁已被证明是一种强有力的刺激分泌的应激反应激素，促肾上腺皮质激素（ACTH）和催乳素。本文综述了我们实验室和其他实验室的研究结果，这些研究结果表明多突触通路参与了对全身尼古丁的神经内分泌反应。它将主要关注下丘脑-垂体-肾上腺（HPA）轴和尼古丁对ACTH分泌的影响，并在相关时提供催乳素分泌的补充信息。数据表明，尼古丁通过中枢机制间接刺激垂体前叶促肾上腺皮质激素的释放。尼古丁似乎并不直接作用于下丘脑室旁核（PVN），而PVN是促肾上腺皮质激素释放激素（CRH）神经元调节ACTH的关键部位。然而，投射到PVN的脑干儿茶酚胺能区域对尼古丁表现出区域选择性和剂量依赖性敏感性，特别是去甲肾上腺素能/肾上腺素能孤束核（NTS）。减少这些儿茶酚胺的调节作用（神经毒性病变，合成酶抑制剂或肾上腺素能受体拮抗剂）导致抑制尼古丁刺激的ACTH分泌。此外，阻断烟碱胆碱能受体（NAchR）在脑干中的拮抗剂，美加明，导致剂量依赖性减少去甲肾上腺素（NE）释放从终端的PVN，并伴随着减少血浆ACTH。这些受体对烟碱激动剂，野靛碱和尼古丁的不同敏感性反映了所涉及的NAchR亚型的异质性。对急性和慢性尼古丁暴露的神经内分泌反应的脱敏特征表明这些NAchR发生了改变。(C)1998爱思唯尔科技有限公司版权所有。
Nicotine has been shown to be a potent stimulus for the secretion of the stress-responsive hormones, adrenocorticotropin (ACTH) and prolactin. This paper reviews the findings by our laboratory and others that demonstrate the polysynaptic pathways involved in the neuroendocrine responses to systemic nicotine. It will focus primarily on the hypothalamo-pituitary-adrenal (HPA) axis and the effect of nicotine on ACTH secretion, with supplementary information on prolactin secretion, where relevant. Data are presented demonstrating that nicotine acts via a central mechanism to stimulate indirectly the release of ACTH from the anterior pituitary corticotropes. Nicotine does not appear to act directly at the hypothalamic paraventricular nucleus (PVN), the site of the corticotropin-releasing hormone (CRH) neurons crucial to the regulation of ACTH. However, brainstem catecholaminergic regions projecting to the PVN showed a regionally selective and dose-dependent sensitivity to nicotine, particularly the noradrenergic/adrenergic nucleus tractus solitarius (NTS). A reduction in the modulatory effect of these catecholamines (by neurotoxic lesion, synthetic enzyme inhibitors or adrenergic receptor antagonists) resulted in an inhibition of nicotine-stimulated ACTH secretion. In addition, blockade of nicotinic cholinergic receptors (NAchRs) in the brainstem by the antagonist, mecamylamine, resulted in a dose-dependent reduction in norepinephrine (NE) release from terminals in the PVN, and a concomitant reduction in plasma ACTH. The differential sensitivity of these receptors to the nicotinic agonists, cytisine and nicotine, reflects the heterogeneity of the NAchR subtypes involved. The desensitization characteristics of the neuroendocrine responses to both acute and chronic nicotine exposure are indicative of an alteration in these NAchRs. (C) 1998 Elsevier Science Ltd. All rights reserved.