Overdistraction and derotation of the scoliotic spine during surgery represent potential complications that could lead to spinal cord dysfunction and paralysis. Neuronal loss and, consequently, the inability to regain function may be attributable to primary damage (eg, mechanical), secondary cell death (eg, such as that produced by ischemia) or a combination of both. Beyond intraoperative recognition and removal of the rods, effective strategies to prevent this neuronal loss have yet to be developed. This emphasizes the need for a clearer understanding of the molecular events that contribute to neuronal injury in the central nervous system. Considerable evidence has indicated that the excitatory transmitter L-glutamate and the N-methyl-D-aspartate (NMDA) excitatory amino acid receptor may contribute to the secondary neuronal death observed in a wide variety of neurological insults, including ischemia. The current investigation was undertaken to elucidate the potential role of the NMDA receptor in spinal cord pathology. Isolated rat spinal cords were exposed to anoxic physiologic solutions in the presence and absence of Ca++, NMDA receptor agonists, and a noncompetitive NMDA receptor antagonist. The extent of neuronal damage was assessed by quantitating the degradation of the cytoskeletal neurofilament protein. A substantial increase in the loss of neurofilament protein was observed in spinal cords exposed to anoxic conditions in the presence of Ca++as compared with the absence of Ca++. Exposure to excitatory amino acid agonists (L-glutamate or NMDA) further potentiated the degradation of the neurofilament protein; an effect that was reversed by a noncompetitive NMDA receptor antagonist. The results support the concept of excitotoxic mediated spinal cord damage and may provide insight into the design of new rational strategies for treating spinal cord injury.
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