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

J Physiol. 1995 Aug 15;487(1):1-16. doi: 10.1113/jphysiol.1995.sp020857.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caffeine / antagonists & inhibitors
  • Caffeine / pharmacology
  • Calcium / metabolism*
  • Calcium / physiology
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / physiology*
  • Electrophysiology
  • Fluorometry
  • Intracellular Membranes / metabolism*
  • Muscle Proteins / physiology*
  • Nerve Fibers / physiology
  • Patch-Clamp Techniques
  • Phosphodiesterase Inhibitors / pharmacology
  • Purkinje Cells / metabolism*
  • Rats
  • Rats, Wistar
  • Reaction Time
  • Ruthenium Red / pharmacology
  • Ryanodine / pharmacology
  • Ryanodine Receptor Calcium Release Channel
  • Synapses / physiology

Substances

  • Calcium Channel Blockers
  • Calcium Channels
  • Muscle Proteins
  • Phosphodiesterase Inhibitors
  • Ryanodine Receptor Calcium Release Channel
  • Ruthenium Red
  • Ryanodine
  • Caffeine
  • Calcium