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促性腺激素细胞的电生理记录。促性腺激素释放激素介导的钙离子通道的证据。

Electrophysiological recordings from gonadotrophs. Evidence for Ca2+ channels mediated by gonadotrophin-releasing hormone.

作者信息

Mason W T, Waring D W

出版信息

Neuroendocrinology. 1985 Sep;41(3):258-68. doi: 10.1159/000124186.

DOI:10.1159/000124186
PMID:2413385
Abstract

The electrophysiological properties of gonadotrophs have been studied in vitro, using the ovine adenohypophyseal pars tuberalis as a naturally enriched source of this cell type. Trypsin-dispersed pars tuberalis cells maintained in primary tissue culture had a membrane potential of -72 +/- 4 mV (mean +/- SEM) and an input resistance of 314 +/- 38 M omega. Spontaneous action potentials were not observed; however, a single spike could be induced by depolarizing current injection. The hypophysiotrophic peptide gonadotrophin-releasing hormone (GnRH) increased membrane voltage fluctuations, but these fluctuations (+/- 5-10 mV) did not induce action potentials or changes in membrane potential or resistance. Power spectra obtained from analysis of this noise indicated that the fundamental event underlying GnRH action has a mean life-time of 38.4 +/- 4.5 ms. The observations that cells incubated in recording medium secreted luteinizing hormone in response to GnRH and that the GnRH-induced increase in voltage noise was inhibited by Ca2+ channel antagonists support the hypotheses (1) that gonadotrophin secretion is initiated by GnRH-induced Ca2+ channel activation and (2) that action potentials are not a prerequisite for gonadotrophin release.

摘要

利用绵羊腺垂体结节部作为这种细胞类型自然富集的来源,对促性腺激素细胞的电生理特性进行了体外研究。原代组织培养中胰蛋白酶分散的结节部细胞的膜电位为-72±4mV(平均值±标准误),输入电阻为314±38MΩ。未观察到自发动作电位;然而,通过去极化电流注入可诱导单个尖峰。促垂体激素促性腺激素释放激素(GnRH)增加了膜电压波动,但这些波动(±5 - 10mV)并未诱导动作电位或膜电位及电阻的变化。对该噪声分析得到的功率谱表明,GnRH作用的基本事件平均寿命为38.4±4.5ms。在记录培养基中孵育的细胞对GnRH有反应分泌促黄体生成素,以及Ca2+通道拮抗剂抑制GnRH诱导的电压噪声增加,这些观察结果支持以下假设:(1)促性腺激素分泌由GnRH诱导的Ca2+通道激活引发;(2)动作电位不是促性腺激素释放的先决条件。

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