PT  - JOURNAL ARTICLE
AU  - Diasynou Fioravante
AU  - Michael H. Myoga
AU  - Michael Leitges
AU  - Wade G. Regehr
TI  - Adaptive Regulation Maintains Posttetanic Potentiation at Cerebellar Granule Cell Synapses in the Absence of Calcium-Dependent PKC
AID  - 10.1523/JNEUROSCI.0683-12.2012
DP  - 2012 Sep 19
TA  - The Journal of Neuroscience
PG  - 13004--13009
VI  - 32
IP  - 38
4099  - http://www.jneurosci.org/content/32/38/13004.short
4100  - http://www.jneurosci.org/content/32/38/13004.full
SO  - J. Neurosci.2012 Sep 19; 32
AB  - 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 PKCα and PKCβ mediate PTP at the calyx of Held synapse, with PKCβ contributing significantly more than PKCα. 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 PKCα/β 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 PKCα/β 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 PKCα or PKCβ 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.