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Ryanodine receptor-mediated intracellular calcium release in rat cerebellar Purkinje neurones

Item Type:Article
Title:Ryanodine receptor-mediated intracellular calcium release in rat cerebellar Purkinje neurones
Creators Name:Kano, M. and Garaschuk, O. and Verkhratsky, A. and Konnerth, A.
Abstract:1. Ryanodine receptor-mediated Ca2+ release was investigated in Purkinje neurones of rat cerebellar slices by using whole-cell patch-clamp recordings combined with fluorometric digital imaging of cytoplasmic Ca2+ concentration ([Ca2+]i). 2. Caffeine caused a transient increase in [Ca2+]i in the somata and dendrites of Purkinje neurones. Caffeine-induced Ca2+ transients were not associated with a membrane inward current and persisted in Ca(2+)-free external solutions, indicating that they are caused by Ca2+ released from intracellular stores. The amplitudes of the caffeine-mediated elevations in [Ca2+]i were strongly dependent on the baseline level of [Ca2+]i. 3. Intracellular application of Ruthenium Red through the patch pipette blocked caffeine-induced Ca2+ transients in Purkinje neurones. Ryanodine when applied either intra- or extracellularly caused a use-dependent block of caffeine-induced Ca2+ release. 4. Depolarization-induced Ca2+ transients were strongly prolonged by caffeine. Several lines of evidence suggest that these prolongations reflect Ca(2+)-induced Ca2+ release. 5. Despite the presence of skeletal muscle type ryanodine receptors in Purkinje neurones, depolarizing pulses failed to induce any changes in [Ca2+]i when the influx of Ca2+ through voltage-gated channels was prevented by using Ca(2+)-free solution, or when applying blockers of voltage-gated Ca2+ channels. 6. Dendritic Ca2+ transients produced by stimulation of the excitatory climbing fibre synaptic input were also prolonged by caffeine, indicating that ryanodine receptor-mediated release of Ca2+ may be involved in synaptic signalling in cerebellar Purkinje neurones. 7. Ryanodine receptor-mediated release of Ca2+ in cerebellar Purkinje neurones can be explained by a model in which release of Ca2+ is strongly facilitated by the co-operative action of Ca2+, caffeine and/or ryanodine. Our results suggest that Ca2+ release in these central neurones becomes prominent only during episodes of intensive electrical activity associated with increased Ca2+ entry.
Keywords:Caffeine, Calcium, Calcium Channel Blockers, Calcium Channels, Electrophysiology, Fluorometry, Intracellular Membranes, Muscle Proteins, Nerve Fibers, Patch-Clamp Techniques, Phosphodiesterase Inhibitors, Purkinje Cells, Reaction Time, Ruthenium Red, Ryanodine, Ryanodine Receptor Calcium Release Channel, Synapses, Animals, Wistar Rats
Source:Journal of Physiology
Publisher:Cambridge University Press
Number:Pt 1
Page Range:1-16
Date:15 August 1995
Official Publication:http://jp.physoc.org/content/487/Pt_1/1.abstract
PubMed:View item in PubMed

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