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促黄体生成素释放激素抑制牛蛙交感神经节中的烟碱传递。

Luteinizing hormone-releasing hormone inhibits nicotinic transmission in bullfrog sympathetic ganglia.

作者信息

Hasuo H, Akasu T

出版信息

Neurosci Res. 1986 Jul;3(5):444-50. doi: 10.1016/0168-0102(86)90036-2.

Abstract

Intracellular and voltage-clamp recordings were made from neurons in bullfrog sympathetic ganglia to investigate the effects of luteinizing hormone-releasing hormone (LH-RH) on nicotinic transmission. LH-RH (50 nM-4 microM) decreased the amplitude of the fast excitatory postsynaptic potential (fast EPSP) in a dose-dependent manner. LH-RH (1-4 microM) reduced the quantal content of the fast EPSP by 60-85%. LH-RH did not change the frequency of the miniature (m) EPSP, but it slightly depressed the mEPSP amplitude. LH-RH (1-4 microM) caused a 22-32% decrease in the amplitude of the acetylcholine-induced synaptic responses due to the iontophoretic application of acetylcholine (ACh) to neurons in the presence of atropine (1 microM). These results suggested that LH-RH decreased nicotinic transmission in the bullfrog sympathetic ganglion, primarily by reducing the release of ACh from the preganglionic nerve terminals.

摘要

采用细胞内和电压钳记录技术,从牛蛙交感神经节的神经元进行记录,以研究促黄体生成素释放激素(LH-RH)对烟碱传递的影响。LH-RH(50 nM - 4 μM)以剂量依赖方式降低快速兴奋性突触后电位(快速兴奋性突触后电位)的幅度。LH-RH(1 - 4 μM)使快速兴奋性突触后电位的量子含量降低了60 - 85%。LH-RH没有改变微小(m)兴奋性突触后电位的频率,但它略微降低了微小兴奋性突触后电位的幅度。在存在阿托品(1 μM)的情况下,通过向神经元离子导入乙酰胆碱(ACh),LH-RH(1 - 4 μM)使乙酰胆碱诱导的突触反应幅度降低了22 - 32%。这些结果表明,LH-RH主要通过减少节前神经末梢乙酰胆碱的释放来降低牛蛙交感神经节中的烟碱传递。

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