Metabotropic glutamate receptor protein alterations after traumatic brain injury in rats

Glutamate toxicity, mediated via ion channel-linked receptors, plays a key role in traumatic brain injury (TBI) pathophysiology. Excessive glutamate r elease after TBI also activates protein G-linked metabotropic glutamate rec eptors (mGluRs), We performed Western blot and immunohistochemical analysis with antibodies for group 1 and 2 mGluRs in hippocampal and cortex tissue at 7 and 15 days after lateral fluid-percussion TBI in rats, Protein homoge nates of brain tissue were separated on 7.5% sodium dodecyl sulfate (SDS)-p olyacrylamide gels, transferred to nitrocellulose, and incubated with eithe r antibodies recognizing both mGluR2 and mGluR3 or antibodies against mGluR 5, Equivalent protein loading of lanes was confirmed by using beta-actin an tibody. Immunoreactive proteins were revealed with enhanced chemiluminescen ce and relative optical density of Western blots quantified by computerized image analysis. At 7 days after TBI, mGluR3 immunobinding ipsilateral to t he fluid-percussion injury was reduced by 28% in hippocampus and 25% in cor tex in comparison with the contralateral hemisphere (p <.05), mGluR5 immuno binding ipsilateral to the fluid-percussion injury was reduced by 20% in hi ppocampus and 27% in cortex (p <.05). At 15 days after TBI, the decreases i n immunobinding were no longer significant, Immunohistochemical staining wi th the same antibodies revealed density changes congruent with the Western blot results. These data suggest that TBI produces an alteration in recepto r protein expression that spontaneously recovers by 15 days after injury.