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

具有固有振荡器的起搏细胞调节许多细胞活动。然而，人们对神经元振荡器的机制及其调节知之甚少。本研究的目的是利用体外电生理技术，阐明盆腔副交感神经节哺乳动物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，分别记录到自发性节律性超极化(SH)和去极化膜振荡(DMO)。作为突触传递的振荡器，我们发现在静息状态下发生的镁敏感性钙内流、钙诱导的钙释放和细胞内钙库泵的钙封存这三个事件的协同作用起着中心作用。作为DMO的离子机制，我们发现钠离子是通过河豚毒素和普鲁卡因阻断的电压门控钠离子通道的主要电荷载体。可能是钠通道激活产生的负斜率电导导致了这种振荡，这一点在海兔神经元中已被提出。当DMO增大或减弱时，细胞分别处于自发放电模式或静止模式。这两种模式可通过乙酰胆碱、去甲肾上腺素等生物物质相互传递。我们还发现，内皮素通过循环GMP依赖的过程启动或增强SH。神经递质对这些振荡的调节提示了哺乳动物自主神经系统中突触调节的一种新模式。

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.