Adaptive Regulation Maintains Posttetanic Potentiation at Cerebellar Granule Cell Synapses in the Absence of Calcium-Dependent PKC

作者：Fioravante Diasynou; Myoga Michael H; Leitges Michael; Regehr Wade G^*

来源：Journal of Neuroscience, 2012, 32(38): 13004-13009.

DOI：10.1523/JNEUROSCI.0683-12.2012

Posttetanic potentiation (PTP) is a transient, calcium-dependent increase in the efficacy of synaptic transmission following elevated presynaptic activity. The calcium-dependent protein kinase C (PKCCa) isoforms PKC alpha and PKC beta mediate PTP at the calyx of Held synapse, with PKC beta contributing significantly more than PKC alpha. It is not known whether PKCCa isoforms play a conserved role in PTP at other synapses. We examined this question at the parallel fiber -> Purkinje cell (PF -> PC) synapse, where PKC inhibitors suppress PTP. We found that PTP is preserved when single PKCCa isoforms are knocked out and in PKC alpha/beta double knock-out (dko) mice, even though in the latter all PKCCa isoforms are eliminated from granule cells. However, in contrast to wild-type and single knock-out animals, PTP in PKC alpha/beta dko animals is not suppressed by PKC inhibitors. These results indicate that PKCCa isoforms mediate PTP at the PF -> PC synapse in wild-type and single knock-out animals. However, unlike the calyx of Held, at the PF -> PC synapse either PKC alpha or PKC beta alone is sufficient to mediate PTP, and if both isoforms are eliminated a compensatory PKC-independent mechanism preserves the plasticity. These results suggest that a feedback mechanism allows granule cells to maintain the normal properties of short-term synaptic plasticity even when the mechanism that mediates PTP in wild-type mice is eliminated.

• 出版日期2012-9-19