カルシウムストアの膜電位変動によるカルシウムオシレーションの同期化

抄録

Synchronous Ca²⁺ oscillation plays essential roles in early neuronal development. The Ca²⁺ oscillation occurs at various parts of the central nervous system including retina even before synapse formation. The Ca²⁺ transients regulate proliferation, axon guidance and neurotransmitter expression. However, it remains unknown how the synchronous Ca²⁺ rises are generated without synaptic inputs. Here I show in embryonic retina that the Ca²⁺ rises are caused by releases of Ca²⁺ from intracellular Ca²⁺ stores, of which synchronization is mediated by high frequency fluctuations in the membrane potential of Ca²⁺ stores. Synchronized Ca²⁺ rises may be caused by synchronous action potentials and ensuing Ca²⁺ influx. However, this was not the case at the early stage of neurodevelopment because, 1) the resting membrane potential of undifferentiated neuroepithelial cells, which show synchronous Ca²⁺ oscillation, was stabilized by lowering input resistance through gap junctions, 2) newborn ganglion cells showed Ca²⁺ influx-dependent repolarization after depolarizing stimuli without any evidence for action potentials, 3) synchronous Ca²⁺ oscillation occurred even in the absence of extracellular Ca²⁺. Fluorescence measurement of store membrane potential with DiOC₅(3) revealed that synchronous voltage fluctuations burst periodically with Ca²⁺ rises. Close apposition of store membranes and plasma membranes in an epithelial structure seemed to allow electrical coupling across the cells. [J Physiol Sci. 2008;58 Suppl:S174]