A wealth of evidence has shown that microglia-associated neuro-inflammation is involved in
the secondary brain injury contributed to the poor outcome after traumatic brain injury (TBI) …

Traumatic brain injury (TBI)-released excessive glutamate resulted in the activation of
glutamate receptors including the metabotropic glutamate receptor 5 (mGluR5). To …

Background Traumatic brain injury initiates biochemical processes that lead to secondary
neurodegeneration. Imaging studies suggest that tissue loss may continue for months or …

Activation of metabotropic glutamate receptor 5 (mGluR5) provided neuroprotection in
multiple central nervous system injury, but the roles of mGluR5 in subarachnoid hemorrhage …

Traumatic brain injury (TBI) induces microglial activation, which can contribute to secondary
tissue loss. Activation of mGluR5 reduces microglial activation and inhibits microglial …

Group I metabotropic glutamate receptors (mGluRs) have been implicated in the
pathophysiology of central nervous system injury, but the role of mGluR5 in traumatic brain …

Objective Excessive release of glutamate from nerve terminals following diffuse brain injury
(DBI) is thought to contribute to neuronal calcium overload leading to calcium-mediated cell …

Both brain native inflammatory cells and infiltrated peripheral white blood cells (WBCs) are
primary participants in the brain inflammatory damage post-TBI. Metabotropic glutamate …

The activation of microglia in response to intracerebral hemorrhagic stroke is one of the
principal components of the progression of this disease. It results in the formation of pro …

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 …