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The mechanisms for the oscillation of membrane potential and current occurred in feline and rabbit parasympathetic neurones

猫和兔副交感神经元膜电位和电流振荡的机制

基本信息

批准号：
04670084
负责人：
NISHIMURA Toshihiko
金额：
$ 1.34万
依托单位：
Kurume 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

项目摘要

Pacemaker cells having an intrinsic oscillator regulate many cellular activities. However little is known the mechanism of the neuronal oscillators and their modulation. The aim of this study was to elucidate the cellular mechanisms for the oscillation of the menbrane potential of mammalian neurones in the pelvic parasympathetic ganglia, utilizing the electrophysiological techniques in vitro. A spontaneous rhythmic hyperpolarization (SH) and a depolarizing membrane oscillation (DMO) were recorded from rabbit and feline parasympathetic neurones, respectively. These two types of the membrane oscillation function as the attenuator or the amplifier for the synaptic transmission.As the oscillator for the SH, we have showed the cooperation of the following three events plays a central role, the magnesium-sensitive Ca-influx occurring at the resting potential, the Ca-induced Ca release and the Ca-sequestration by the pump of the intracellular Ca-stores. The sequential activation and inactivation of these three events cause the oscillation of cytoplasmic concentration of Ca that activates the Ca-dependent channels in the plasma membrane, resulting in the SH.As the ionic mechanism for the DMO, we have found that sodium ions are the main charge carrier through the voltage-gated sodium channels that are blockd by tetrodotoxin and procaine. Probably negative slope conductance occurred by activation of the sodium channels is responsible for the oscillation, as has been suggested in Aplysia neurones. When the DMO is augmented or attenuated, the cells are in a spontaneous firing mode or a quiescent mode, respectively. These two modes could be transfered each other by biogenic substances, such as acetylcholine and norepinephrine. We also found that endothelin initiated or augmented the SH through cyclic GMP-dependent process. The modulation of these oscillations by neurotransmitters suggests a new mode of the synaptic modulation in the mammalian autonomic nervous system.

具有内在振荡器的起搏细胞调节许多细胞活动。然而，很少有人知道的神经元振荡器及其调制的机制。本研究的目的是利用离体电生理技术阐明哺乳动物盆副交感神经节神经元膜电位振荡的细胞机制。在兔和猫的副交感神经元上分别记录到自发节律性超极化（SH）和去极化膜振荡（DMO）。这两种类型的膜振荡在突触传递中起着衰减或放大的作用，而作为SH的振荡器，我们已经证明以下三个事件的协同作用起着核心作用：静息电位下发生的镁敏感性Ca内流，Ca诱导的Ca释放和细胞内Ca库泵的Ca螯合。这三个事件的顺序激活和失活引起细胞质Ca浓度的振荡，激活质膜中的Ca依赖性通道，导致SH。作为DMO的离子机制，我们发现钠离子是通过电压门控钠通道的主要电荷载体，该通道被河豚毒素和普鲁卡因阻断。可能是由于钠通道的激活而发生的负斜率电导是振荡的原因，正如在动脉瘤神经元中所提出的那样。当DMO增强或衰减时，细胞分别处于自发放电模式或静止模式。这两种模式可以通过乙酰胆碱和去甲肾上腺素等生物源物质相互传递。我们还发现，内皮素启动或增强SH通过循环GMP依赖的过程。神经递质对这些振荡的调制提示了哺乳动物自主神经系统中突触调制的一种新模式。