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Brain mechanism regulating pulsatile secretion of luteinizing hormone-releasing hormone

调节黄体生成素释放激素脉动分泌的脑机制

基本信息

批准号：
04660289
负责人：
MAEDA Kei-ichiro
金额：
$ 1.34万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04660289/
关键词：
Luteinizing hormone (LH)LH-releasing hormone Stress Ovary Hypothalamus Pituitary LHパルス神経内分泌

项目摘要

We proposed hypothesis that the LHRH pulse generator consists of non-LHRH neurons and is located in the MBH.The site at which the LHRH pulse generator acts LHRH neurons could be the median eminence where the terminals of LHRH neurons are concentrated, because pulsatile LH secretion was not impaired by the complete deafferentation which separated the LHRH neuronal terminals from the cell bodies located in the preoptic / septum region. To explore this possibility, we examined in vitro LHRH release from the median eminence tissues taken from ovariectomized rates and incubated with various neurotransmitters, such as monoamines or excitatory amino acids (EAAs). Any monoamines, such as norepinephrine, dopamine, serotonin or histamine, did not induce in vitro LHRH release from the median eminence tissues at a physiological dose. On the other hand, EAA agonists, such as glutamate, NMDA, AMPA or kainate, increased in vitro LHRH release from the tissues, suggesting that the endogenous EAAs released into the median eminence generate the pulsatile LHRH release. We then tried to block LH pulses by implanting excitatory amino acid antagonists into the median eminence to test whether the endogenous EAAs are involved in generating pulsatile LHRH release at the median eminence. Both CPP, a NMDA-type EAA receptor antagonist, and DNQX, a non-NMDA-type receptor antagonist, were effective in decreasing pulsatile LH secretion, although the suppression was not complete. The present results strongy support our hypothesis that pulsatile LHRH release is regulated at the LHRH neuronal terminals located in the median eminence probably through EAA receptors.

我们提出假设LHRH脉冲发生器由非LHRH神经元组成，位于MBH。LHRH脉冲发生器作用于LHRH神经元的位置可能是LHRH神经元末梢集中的正中隆起，因为LHRH神经元末梢与位于视前/隔区的细胞体完全脱神经并没有损害脉动性LH分泌。为了探索这种可能性，我们检测了卵巢切除后正中嵴组织中LHRH的体外释放，并与各种神经递质（如单胺或兴奋性氨基酸（EAAs））孵育。任何单胺类药物，如去甲肾上腺素、多巴胺、血清素或组胺，在生理剂量下都不能诱导正中隆起组织体外释放LHRH。另一方面，谷氨酸、NMDA、AMPA或kainate等EAA激动剂增加了体外组织中LHRH的释放，表明内源性EAA释放到正中隆起产生搏动性LHRH释放。然后，我们尝试通过在正中隆起植入兴奋性氨基酸拮抗剂来阻断LH脉冲，以测试内源性eaa是否参与在正中隆起产生脉动性LHRH释放。nmda型EAA受体拮抗剂CPP和非nmda型受体拮抗剂DNQX均能有效降低脉动性LH分泌，但抑制不完全。目前的结果有力地支持了我们的假设，即搏动性LHRH释放可能是通过EAA受体在位于中央隆起的LHRH神经元末梢进行调节的。