Postsynaptic scaffold protein Homer 1a protects against traumatic brain injury via regulating group I metabotropic glutamate receptors

Excitotoxicity Postsynaptic density Long-term depression
DOI: 10.1038/cddis.2014.116 Publication Date: 2014-04-10T14:34:15Z
ABSTRACT
Traumatic brain injury (TBI) produces excessive glutamate, leading to excitotoxicity via the activation of glutamate receptors. Postsynaptic density scaffold proteins have crucial roles in mediating signal transduction from receptors their downstream mediators. Therefore, studies on mechanisms underlying regulation by can uncover new treatments for TBI. Here, we demonstrated that postsynaptic protein Homer 1a was neuroprotective against TBI vitro and vivo, this neuroprotection associated with its effects group I metabotropic (mGluRs). Upon further study, found mainly affected neuronal induced mGluR1 after also influenced mGluR5 function when activity restored. The ability disrupt mGluR-ERK signaling contributed regulate functions traumatic injury. Intracellular Ca2+ PKC were two important factors involved mediation 1a. These results define as a novel endogenous agent
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