Ca2+signals underlying synaptic plasticity in cerebellar Purkinje neurones

Abstract

Cerebellar Purkinje neurones display two forms of synaptic plasticity that critically depend on a transient increase in intracellular Ca²⁺for their induction. They are a long-term depression (LTD) of the excitatory glutamatergic parallel fibre input, and a long-lasting potentiation, called rebound potentiation (RP), of inhibitory inputs mediated by γ-aminobutyric acid. A number of mechanisms could participate in the increase in cytoplasmic Ca²⁺concentration. These include Ca²⁺entry from the extracellular space through voltage-gated Ca²⁺channels and ionotropic glutamate receptors, and Ca²⁺release from intracellular stores sensitive to Ca²⁺and inositol trisphosphate. The evidence obtained from cerebellar slices suggests that, of these, the activation of P-type voltage-gated Ca²⁺channels by membrane depolarization provides the predominant amount of Ca²⁺necessary for the induction of LTD and RP.