In the taste bud, a tight associate of 50-100 taste cells of different types, extracellular volume is less than that of the cytoplasm by two orders of magnitude. By that, electrical activity of taste bud cells, which is associated with redistribution of physiologically important ions between the cell cytoplasm and external medium, can entail substantial variations of extracellular ions, including Ca2+. Type III taste cells form classical chemical synapses and release neurotransmitter by employing exocytosis that is triggered by Ca2+ ions entering through voltage-gated (VG) Са2+- channels. The depletion of external Са2+ should result in a decreased release of neurotransmitter in response to the same taste stimulus, thus non-adequately conveying taste information to the brain. One therefore can expect the existence of certain that provides invariance of neurotransmitter release from type III cells within a physiologically relevant range of concentrations of external Са2+. To examine this idea, we analyzed here the dependence of VG Са2+-currents in taste cells on extracellular Са2+. As was found, VG Са2+-current magnitude versus concentration of bath Са2+ exhibited a plateau in the range of 1-2 mM. In addition, we monitored intracellular Ca2+ signals produced by Ca2+ influx through VG Ca2+- channels upon cell depolarization. It turned out that the magnitude of VG Ca2+ transients was weakly or even negligibly dependent on external Ca2+ varied from 0,5 to 5 mM. These findings validate the idea that a certain mechanism regulates activity of VG Са2+-channels to ensure the invariance of Са2+ influx triggering neurotransmitter release at variable extracellular Ca2+.
2+-sensing receptor
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