Regulation of inhibitory synaptic plasticity in a Purkinje neuron.

Inhibitory synapses on Purkinje cells show synaptic plasticity such as rebound potentiation (RP), which seems to contribute to refined information processing in the cerebellar cortex. Recent progress in the study on regulation mechanism of RP is reported. RP is induced by depolarization of a Purkinje cell and expressed as the increased postsynaptic responsiveness to GABA. RP might work as a homeostatic mechanism to maintain activity of a Purkinje cell sensing the strength of heterosynaptic excitatory inputs. However, there is a homosynaptic mechanism to regulate RP. RP is suppressed by the GABAergic transmission occurring during depolarization. Elaborate molecular regulation mechanism of RP induction, including GABA(B) receptors, Ca(2+), cyclic adenosine 3',5'-monophosphate (cAMP), kinases such as Ca(2+)- and calmodulin-dependent kinase II and protein kinase A, and protein phosphatases such as PP1 and PP2B, has been clarified. Application of systems biological analyses combined with electrophysiological experiments has revealed a critical role of phosphodiesterase 1 in determination of the Ca(2+) signal to induce RP.