TY - JOUR T1 - Activation of Metabotropic Glutamate Receptor Subtype mGluR1 Contributes to Post-Traumatic Neuronal Injury JF - The Journal of Neuroscience JO - J. Neurosci. SP - 6012 LP - 6020 DO - 10.1523/JNEUROSCI.16-19-06012.1996 VL - 16 IS - 19 AU - Alexey Mukhin AU - Lei Fan AU - Alan I. Faden Y1 - 1996/10/01 UR - http://www.jneurosci.org/content/16/19/6012.abstract N2 - The role of phospholipase C-coupled (group I) metabotropic glutamate receptors (mGluR1 and mGluR5) in post-traumatic neuronal injury was examined using rat in vivo and in vitro models. Traumatic injury to mixed neuronal/glial cultures induced phosphoinositide hydrolysis and caused neuronal death. Pharmacological blockade of group I receptors significantly reduced these effects in vitro and decreased neurological deficits as well as neuronal loss produced by traumatic brain injuryin vivo. In contrast, activation of group I receptors by a specific agonist in vitro exacerbated post-traumatic neuronal death in a dose-dependent manner. Antisense oligodeoxynucleotide directed to mGluR1, but not to mGluR5, was neuroprotective in vitro, although each oligodeoxynucleotide reduced the respective receptor-stimulated accumulation of inositol phosphates to a similar degree. Together, these findings suggest that activation of mGluR1 contributes to post-traumatic neuronal injury and that mGluR1 antagonists may have therapeutic potential in brain injury. ER -