| Research Abstract |
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.
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