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METABOTROPIC GLUTAMATE RECEPTOR IN TRAUMATIC AXONAL INJURY IN THE RAT

Departments of Anesthesia and Surgery, St. Michael's Hospital and The University Health Network, Toronto, Ontario

INTRODUCTION

Following SCI and TBI, secondary injury mechanisms promote axonal damage. We hypothesized that the mGluR1 and mGluR5 receptors are involved in these processes and sought to determine their role in post-traumatic axonal dysfunction.

METHODS

Western immunoblotting and immunohistochemistry were performed on rat corpus callosum following fluid percussion TBI. Compound action potentials (CAPs) were recorded in dorsal columns after SCI and corpus callosum brain slices following TBI. [Ca²⁺]_i fluorescence was measured in spinal cord slices in wild-type and mGluR1-/- mice.

RESULTS

Immunoblots showed increase ßAPP at 24hr, calpain activation at 30min and 24hr, and NF200 breakdown at 7d following TBI. Axonal electrophysiological recovery following in vitro SCI and TBI improved with Group 1 blockade using PHCCC. [Ca²⁺]_i imaging showed a reduction in post-traumatic [Ca²⁺]_i rises with PHCCC and mGluR1 gene deletion. Following TBI, Group 1 mGluRs blockade led to a CAP recovery of 77.1 ± 10.2% compared to 37.6 ± 5.4% in controls. mGluR1 blockade led to a recovery of 52.9 ± 7.4%, while mGluR5 blockade resulted in 63.2 ± 10.3% recovery. All results were statistically significant (p<0.01).

CONCLUSIONS

Our results suggest that Group1 mGluRs are involved in axonal dysfunction following neurotrauma. Combined mGlur1 and mGlur5 blockade leads to a better axonal recovery than blockade of each receptor alone.

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