Membrane potential changes caused by thyrotropin-releasing hormone in the clonal GH3 cell and their relationship to secretion of pituitary hormone.
Membrane potential changes caused by thyrotropin-releasing hormone in the clonal GH3 cell and their relationship to secretion of pituitary hormone.
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克隆GH3细胞促甲状腺素释放激素引起的膜电位变化及其与垂体激素分泌的关系。
DOI：
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发表时间：
1979
影响因子：
11.1
通讯作者：
N. Kimura
中科院分区：
文献类型：
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作者：
S. Ozawa;N. Kimura
用连续记录细胞内电位的方法，研究了促甲状腺激素释放激素（TRH）对克隆大鼠垂体前叶细胞（GH 3）膜电特性的影响。TRH的应用，刺激泌乳素和生长激素从GH3细胞的释放，引起细胞膜的瞬时超极化，随后在大多数测试的细胞中，动作电位的产生持续一段时间的增强。瞬时超极化是由于膜对K+的电导增加。峰电位产生的增强不是由于膜去极化。在易化过程中，细胞膜的输入电阻增加。因此TRH易化作用的机制不同于传统的兴奋性神经递质的机制。TRH增强尖峰的产生，从而促进Ca 2+从胞外进入胞内空间（GH3细胞的动作电位具有Ca 2+成分）并刺激激素的释放。这一观点得到了以下观察结果的支持：钴离子阻断了这些细胞中的钙峰，完全消除了TRH对催乳素和生长激素释放的刺激作用。
Effects of thyrotropin-releasing hormone (TRH; thyroliberin) on membrane electrical properties were studied in the clonal rat anterior pituitary cell (GH3) by continuous recording of the intracellular potential. Application of TRH, which stimulates the release of prolactin and growth hormone from the GH3 cell, elicited a transient hyperpolarization of the cell membrane followed by an enhancement of the generation of action potentials for an extended period in the majority of cells tested. The transient hyperpolarization was due to an increase of the membrane conductance to K+. The enhancement of the spike generation was not due to membrane depolarization. The input resistance of the cell membrane was found to be increased during the facilitation. Thus the mechanism of the facilitatory action of TRH is different from the mechanisms of conventional excitatory neurotransmitters. TRH enhances the spike generation, thus promoting Ca2+ entry from extra- to intracellular space (the action potential of the GH3 cell has a Ca2+ component) and stimulating the release of hormones. This notion is supported by the observation that cobalt ions, which block the calcium spike in these cells, completely abolished the stimulatory effect of TRH on the release of prolactin and growth hormone.