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

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

The Group I metabotropic glutamate receptor 5 (mGluR5) can modulate addiction, pain, and
neuronal cell death. Expression of some mGluRs, such as Group II and III mGluRs, has been …

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 …

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

Microglial-related factors have been implicated in the signaling cascades that contribute to
neuronal cell death in various neurodegenerative disorders. Thus, strategies that reduce …

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

Background Activation of metabotropic glutamate receptor 5 (mGluR5) by (RS)-2-chloro-5-
hydroxyphenylglycine (CHPG) was shown to suppress microglia activation and decrease …

Previous studies have demonstrated that antagonists of mGluR1, but not mGluR5, are
neuroprotective in models of cerebral ischemia. To investigate the individual roles of mGlu1 …