A unique PDZ ligand in PKCalpha confers induction of cerebellar long-term 
synaptic depression.

Leitges, M.; Kovac, J.; Plomann, M.; Linden, D. J.

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A unique PDZ ligand in PKCalpha confers induction of cerebellar long-term synaptic depression.

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Leitges, M.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

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Kovac, J.
Research Group on Circadian Rythms, MPI for biophysical chemistry, Max Planck Society;

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Citation

Leitges, M., Kovac, J., Plomann, M., & Linden, D. J. (2004). A unique PDZ ligand in PKCalpha confers induction of cerebellar long-term synaptic depression. Neuron, 44(4), 585-594. Retrieved from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15541307.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-EBC7-B

Abstract

Induction of cerebellar long-term depression (LTD) requires a postsynaptic cascade involving activation of mGluR1 and protein kinase C (PKC). Our understanding of this process has been limited by the fact that PKC is a large family of molecules, many isoforms of which are expressed in the relevant postsynaptic compartment, the cerebellar Purkinje cell. Here, we report that LTD is absent in Purkinje cells in which the alpha isoform of PKC has been reduced by targeted RNA interference or in cells derived from PKCalpha null mice. In both of these cases, LTD could be rescued by expression of PKCalpha but not other PKC isoforms. The special role of PKCalpha in cerebellar LTD is likely to derive from its unique PDZ ligand (QSAV). When this motif is mutated, PKCalpha no longer supports LTD. Conversely, when this PDZ ligand is inserted in a nonpermissive isoform, PKCgamma, it confers the capacity for LTD induction.