Group II metabotropic glutamate receptor activation attenuates traumatic neuronal injury and improves neurological recovery after traumatic brain injury

We examined the effects of modulating group II metabotropic glutamate receptors (mGluRs) on traumatic neuronal injury us-ing both in vitro and in vivo models. Treatment with various selective group II mGluR agonists significantly decreased lac-tate dehydrogenase release, a marker of cell death, after trau-matic injury to rat neuronal-glial cultures; injury-induced in-creases in cyclic AMP and glutamate levels were also significantly reduced by a group II agonist. The neuroprotective effects of group II agonists were markedly attenuated by co-administration of a group II antagonist or a membrane-perme-able cyclic AMP analog and were additive to those provided by an N-methyl-D-aspartate receptor antagonist or a selective group I mGluR antagonist. Administration of a group II mGluR agonist 30 min after lateral fluid percussion-induced brain injur