Physiological functions of nitric-oxide induced calcium-release in central nervous systems

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The aim of this project is to examine the mechanism and functional role of nitric oxide-induce Ca2+ elevation in central neurons. In mouse cerebellar Purkinje cells, application of nitric oxide (NO) induced intracellular Ca^<2+> levels, and the elevation was revealed to be dependent on Ca^<2+> release from intracellular store. NO-induced Ca^<2+> increase was induced also by physiological patterns of neuronal activity which induces synaptic plasticity. Furthermore, the condition which blocks NO-induced Ca^<2+> increase also impaired the synaptic plasticity. There results indicate that NO-induced Ca^<2+> release is essential for the induction of synaptic plasticity in the cerebellum.