Design, synthesis, and biological evaluation of novel N6-Isopentenyladenosine Analogues

Increases in intracellular [Ca2+] occur synchronously between cells in the neuroepithelium. If neuroepithelial cells were capable of generating action potentials synchronized by gap junctions (direct current electrical coupling), the influx of Ca2+ through voltage-activated Ca2+ channels would lead to a synchronous increase in intracellular [Ca2+]. However, no action potential is generated in neuroepithelial cells, and the [Ca2+] increase is instead produced by the release of Ca2+ from intracellular Ca2+ stores. Recently, synchronous fluctuations in the membrane potential of Ca2+ stores were recorded using an organelle-specific voltage-sensitive dye. On the basis of these recordings, a capacitative [alternating current (AC)] electrical coupling model for the synchronization of voltage fluctuations of Ca2+ store potential was proposed [Yamashita M (2006) FEBS Lett580, 4979-4983; Yamashita M (2008) FEBS J275, 4022-4032]. Ca2+ efflux from the Ca2+ store and K+ counterinflux into the store cause alternating voltage changes across the store membrane, and the voltage fluctuation induces ACs. In cases where the store membrane is closely apposed to the plasma membrane and the cells are tightly packed, which is true of neuroepithelial cells, the voltage fluctuation of the store membrane is synchronized between the cells by the AC currents through the series capacitance of these membranes. This article provides a short review of the model and its relationship to the structural organization of the Ca2+ store. This is followed by a discussion of how the mode of synchronization of [Ca2+] increase may change during central nervous system development and new molecular insights into the synchronicity of [Ca2+] increase.