Quantitative study of mutual relationships involving Ca channel, cytosolic Ca concentration, Na-Ca exchange and Na-K ATPase

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Excitation of neuronal and muscular cells is triggered by depolarization-induced Ca^<2+> entry to the cytoplasm. The release of neurotransmitter substance from presynaptic terminals is mediated by similar mechanisms. As such, Ca^<2+> is an internal messenger, with its cytosolic concentration normally maintained at the submicromolar level. The Ca buffering can be subserved by cytoplasmic ca ion stores. No less important for the Ca regulation is the Na-Ca exchange machinery that excludes calcium ions by letting Na ions move into the cell. The passive Na influx may also result from voltage-gated as well as drug-operated channels. Thus. Na ions also need to be expelled. This physiologic demand is fulfilled by the Na-K pump. This study was done in the context of intracellular ion homeostasis recaputulated above.Voltage clamp experiments using patch pippete were made on solitary horizontal cells isolated enzymatically from the goldfish retina. Since the physiological dynamic range of these non-spiking second-order visual neurons overlaps the membrane voltage region that activates the voltage-gated Ca channel, some mechanism needs to exist to drive out Ca ions. A series of experiments involving the Co test and Na-free substitution showed that the Ca extrusion is subserved by the Na-Ca exchanger. Another set of experiments including by caffeine application indicated the presence of internal calcium stores having a storage capacity of as much as several mM. In this regard, the endplasmic reticulum probably plays a major role. Some regulatory system is required with respect to Na ions as well, to compensate for three types of Na influx: TTX-sensitive one, the Na-Ca exchange component and synaptic current mediated by an excitatory neurotransmitter from photoreceptor terminals. the Ns-KATP ase ope rates for this requirement. Evidence being provided by an ouabain experiment.