English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

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

MPS-Authors
/persons/resource/persons15429

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

/persons/resource/persons15368

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

Locator
There are no locators available
Fulltext (public)

270923.pdf
(Publisher version), 0B

Supplementary Material (public)
There is no public supplementary material available
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: http://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.