Deactivation of l-type ca current by inhibition controls ltp at excitatory synapses in the cerebellar nuclei

Abigail L. Person*, Indira M. Raman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Long-term potentiation (LTP) of mossy fiber EPSCs in the cerebellar nuclei is controlled by synaptic inhibition from Purkinje neurons. EPSCs are potentiated by a sequence of excitation, inhibition, and disinhibition, raising the question of how these stimuli interact to induce plasticity. Here, we find that synaptic excitation, inhibition, and disinhibition couple to different calcium-dependent signaling pathways. In LTP induction protocols, constitutively active calcineurin can replace synaptic excitation, and constitutively active α-CaMKII can replace calcium influx associated with resumption of spiking upon disinhibition. Additionally, nimodipine can replace hyperpolarization, indicating that inhibition of firing decreases Ca influx through L-type Ca channels, providing a necessary signal for LTP. Together, these data suggest that potentiation develops after a calcineurin priming signal combines with an α-CaMKII triggering signal if and only if L-type Ca current is reduced. Thus, hyperpolarization induced by synaptic inhibition actively controls excitatory synaptic plasticity in the cerebellar nuclei.

Original languageEnglish (US)
Pages (from-to)550-559
Number of pages10
Issue number4
StatePublished - May 2010


  • Molneuro

ASJC Scopus subject areas

  • Neuroscience(all)


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