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

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

Traumatic brain injury (TBI) causes microglial activation and related neurotoxicity that
contributes to chronic neurodegeneration and loss of neurological function. Selective …

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) …

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 …

We have previously shown that treatment with a mGluR5 positive allosteric modulator (PAM)
is neuroprotective after experimental traumatic brain injury (TBI), limiting post‐traumatic …

Several previous studies utilizing selective pharmacological antagonists have demonstrated
that type 5 metabotropic glutamate receptors (mGluR5) are potential therapeutic targets for …

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 …

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

Objective Activation of metabotropic glutamate receptor 5 (mGluR5) has neuroprotective
properties in vitro and has been reported to limit postischemic lesion volume in vivo …