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Calpain product of WT‐CRMP2 reduces the amount of surface NR2B NMDA receptor subunit
Author(s) -
Bretin Sylvie,
Rogemond Véronique,
Marin Philippe,
Maus Marion,
Torrens Yvette,
Honnorat Jérôme,
Glowinski Jacques,
Prémont Joël,
Gauchy Christian
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.03969.x
Subject(s) - nmda receptor , calpain , neuroscience , protein subunit , agonist , glutamatergic , excitotoxicity , microbiology and biotechnology , synaptic plasticity , receptor , chemistry , biology , glutamate receptor , biochemistry , enzyme , gene
The brain is particularly vulnerable to ischaemia; however, neurons can become tolerant to ischaemic insult. This tolerance has been shown to involve activation of NMDA receptors, but its mechanisms have not yet been fully elucidated. Using a preconditioning protocol, we show that neurons surviving to a transient NMDA exposure become resistant to the glutamatergic agonist. Using a proteomic approach, we found that alterations of the protein pattern of NMDA‐resistant neurons are restricted mainly to the five collapsin response mediator proteins (CRMPs). A sustained increase in calpain activity following NMDA treatment is responsible for the production of cleaved CRMPs. Finally, we provide evidence for the involvement of the cleaved form of WT‐CRMP2 in the down‐regulation of NR2B. Our data suggests that, beside their role in neuronal morphogenesis, CRMPs may contribute to neuronal plasticity.