[Changes of N-methyl-D-aspartate receptor in spinal cord after trauma]

N-methyl-D-aspartate (NMDA) receptor-mediated events have implicated in the pathophysiology of posttraumatic spinal cord injury. In the present study, [3H] CPP was used as ligand to analyse the changes in NMDA receptor-binding sites in synaptic plasma membranes (SPM) isolated from rat spinal cord after impact trauma at T10. Radio-binding assays of [3H] CPP showed a specific and saturable binding site for [3H] CPP in spinal cord tissue. Scatchard analysis revealed the binding of [3H] CPP has one site with low affinity (Kd = 3.51 < or = 0.26 nM) and binding density (Bmax = 662.82 < or = 47.59 fmol/mg protein). [3H] CPP binding to NMDA receptor at the thoracic segment was significantly (P < 0.01) decreased posttrauma. Time-course studies demonstrated significantly decrease in the binding of [3H] CPP at 4 h after spinal cord injury with recovery by 24 h. Scatchard analysis results indicate that the posttrauma decrease of [3H] CPP-binding resulted from alteration in receptor binding density The data from the present study provided further evidence for a role for NMDA receptor-mediated mechanisms in the pathological consequences of spinal cord injury. The acute reduction in [3H] CPP-binding after trauma may reflect down-regulation of NMDA receptor as a consequence of posttraumatic glutamate release and may serve to limit excitotoxin-induced injury.