Excitatory amino acid receptor subtype binding following traumatic brain injury

Sprague-Dawley rats were subjected to a moderate level (2.2 atm) of traumatic brain injury (TBI) using fluid percussion. Injured animals were allowed post-trauma survival periods of 5 min, 3 and 24 h. Regional glutamate receptor subtype binding was assessed with quantitative autoradiography in each group for N-methyl- d-aspartate (NMDA), quisqualate and kainate receptor subpopulations at approximately the −3.8 bregma level and compared to a sham control group. [ 3H]glutamate binding to the NMDA receptor was significantly ( P < 0.05) decreased at 3 h post-TBI in the hippocampal CA1 stratum radiatum, the molecular layers of the dentate gyri and the outer (layers 1–3) and inner (layers 5 and 6) overlying neocortex. NMDA receptor binding was significantly reduced in layers 5 and 6 of the neocortex at all post-trauma survival times but no further differences were seen in the hippocampi. No significant changes were observed with [ 3H]AMPA binding to quisqualate receptors and [ 3H]KA binding was significantly reduced only in layers 5 and 6 of the neocortex at 24 h after TBI. These data further confirm the pathological involvemnt of the NMDA receptor complex in brain regions selectively vulnerable to moderate levels of TBI in this model.