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Role for microsomal Ca storage in mammalian neurones?


Alterations in the intracellular concentration of calcium ions ([Ca2+]i) are increasingly being found to be associated with regulatory functions in cells of all kinds. In muscle, an elevation of [Ca2+]i, is the final link in excitation–contraction coupling1–3 while at nerve endings and in secretory cells, similar rises in [Ca2+]i, are thought to mediate exocytosis4,5. The discovery of calcium-activated ion channels6,7 indicated a role for intracellular calcium in the regulation of membrane excitability. Calcium transients associated with either intracellular release or the inward movement of Ca2+ across the membrane have been recorded in molluscan neurons8,9 and more recently in neurones of bullfrog sympathetic ganglia10. Here, we report the first recordings of calcium transients in single mammalian neurones. In these experiments we have found that the methylxanthine, caffeine, causes the release of calcium from a labile intracellular store which can be refilled by Ca2+ entering the cell during action potentials.

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Neering, I., McBurney, R. Role for microsomal Ca storage in mammalian neurones?. Nature 309, 158–160 (1984).

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