Role for microsomal Ca storage in mammalian neurones?

Abstract

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 coupling^1–3 while at nerve endings and in secretory cells, similar rises in [Ca²⁺]_i, are thought to mediate exocytosis^4,5. The discovery of calcium-activated ion channels^6,7 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 neurons^8,9 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.