Purkinje Neurons: Synaptic Plasticy

Abstract

After three decades of research, it is now well established that molecular mechanisms underlying cerebellar motor learning lead to activity-dependent changes in synaptic strength, such as long-term depression (LTD) and longterm potentiation (LTP) at cerebellar parallel fiber (PF)-Purkinje cell (PC) glutamatergic synapses. This review focuses on mechanisms of these longterm changes in synaptic efficacy, even though short-term forms of synaptic plasticity also exist at these synapses and may also contribute to neural processing of information within the cerebellum. In light of the newly obtained experimental data from transgenic mice, it will also be discussed as to why these forms of synaptic plasticity are proposed as the cellular basis for error-driven learning and memory in the motor system.

Cerebellar synapse properties and cerebellum-dependent motor and non-motor performance in Dp71-null mice

“…3 A). CF-triggered complex spikes generate prominent dendritic Ca 2+ increases in PCs mediating several types of long-term plasticity at PF synapses ( Ohtsuki et al, 2009 ; Daniel and Crepel, 2012 ; Hoxha et al, 2016 ). Moreover, homosynaptic long-term depression (LTD) occurs at CF-PC synapses ( Hansel and Linden, 2000 ), thus confirming the widespread notion that CF activity governs various types of plasticity that can modulate PC output ( Ohtsuki et al, 2009 ).…”

Native Presynaptic Metabotropic Glutamate Receptor 4 (mGluR4) Interacts with Exocytosis Proteins in Rat Cerebellum

“…The most compelling demonstration for a physiological function of presynaptic mGluR4 is found at the glutamatergic synapses between parallel fibers and Purkinje cells in the rodent cerebellar cortex. At these synapses, pharmacological activation of these receptors acutely depresses excitatory transmission and inhibits presynaptic calcium influx (7,8). In the rodent cerebellum, depression of parallel fiberPurkinje cell excitatory transmission is exclusively due to mGluR4 (8).…”