Expression and cell distribution of metabotropic glutamate receptor 5 in the rat cortex following traumatic brain injury

Traumatic brain injury (TBI)-released excessive glutamate resulted in the activation of glutamate receptors including the metabotropic glutamate receptor 5 (mGluR5). To investigate the expression and cell distribution of mGluR5 in the rat cortex following TBI, western blot and quantitative real-time PCR were used to study the protein and mRNA level of mGluR5 respectively while immunohistochemistry analysis and double immunofluorescence with neural cell marker were used to define the cell distribution of mGluR5. Furthermore, we examined the effects of post-TBI administration of (R,S)-2-chloro-5-hydroxyphenylglycine (CHPG), a selective mGluR5 agonist, on the neuronal degeneration in the cortex. In the present study, we found that the protein level of mGluR5 was up-regulated by traumatic brain injury, while TBI-induced mGluR5 mRNA expression displayed biphasic changes with up-regulation in the early time and down-regulation in the late time after TBI. And neuron, astrocyte and microglia in the cortex after TBI all expressed mGluR5. Moreover, CHPG treatment significantly reduced the number of degenerating neurons detected by Fluoro-Jade C staining. These findings demonstrate that expression of mGluR5 differentially changes both spatially and temporally after TBI and may be related to the neuroprotection after TBI. Therefore, understanding the expression and cell distribution of mGluR5 after TBI may give insight into pathophysiology after TBI and provide a new target for the therapy of TBI.