Purkinje cell intrinsic excitability increases after synaptic long term depression

Coding in cerebellar Purkinje cells not only depends on synaptic plasticity but also on their intrinsic membrane excitability. We performed whole cell patch clamp recordings of Purkinje cells in sagittal cerebellar slices in mice. We found that inducing long term depression (LTD) in the parallel fiber (PF) to Purkinje cell (PC) synapses results in an increase in the gain of the firing rate response. This increase in excitability is accompanied by an increase in the input resistance and a decrease in the amplitude of the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel mediated voltage sag. Application of a HCN channel blocker prevents the increase in input resistance and excitability without blocking the expression of synaptic LTD. We conclude that induction of PF-PC LTD is accompanied by an increase in excitability of Purkinje cells through down-regulation of the HCN mediated h current. We suggest that HCN down-regulation is linked to the biochemical pathway that sustains synaptic LTD. Given the diversity of information carried by the parallel fiber system, we suggest that changes in intrinsic excitability enhance the coding capacity of the Purkinje cell to specific input sources.

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