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  • Title: [Glutamate neurotoxicity during spinal cord ischemia--neuroprotective effects of glutamate receptor antagonists].
    Author: Nakamichi T.
    Journal: Jpn J Thorac Cardiovasc Surg; 1998 Sep; 46(9):854-9. PubMed ID: 9796285.
    Abstract:
    Evidence is accumulating that glutamate, a major neurotransmitter, exerts potent neurotoxic activity during ischemia. In our laboratory, a delayed-onset paraplegia model using rabbits has been developed and described. The severity of the ischemic event in this model, i.e., extracellular glutamate overload, is believed to influence the etiology of this borderline lesion. We hypothesized that glutamate receptor antagonists (MK-801, NBQX) would attenuate the delayed neuronal dysfunction that follows spinal cord ischemia. Infrarenal aortic segments from 18 New Zealand white rabbits were isolated for 5 minutes and infused at a rate of 2 ml/min. Group I (n = 6) received normothermic L-glutamate (20 mM). Group II (n = 6) received 3 mg of MK-801 and normothermic L-glutamate (20 mM). Group III (n = 6) received 3 mg of NBQX and normothermic L-glutamate (20 mM). Neurologic function was assessed at 6, 24, and 48 hours after surgery according to the modified Tarlov scale. After 48 hours, the rabbits were euthanized and spinal cords were harvested for histologic examination. The neurologic function of three rabbits in group I showed acure paraplegia and the other three showed delayed-onset paraplegia, whereas all group II animals had nearly intact neurologic function and all group III animals showed mild neurologic disturbance. Histologic examination of spinal cords from rabbits in group I showed evidence of moderate spinal cord injury with necrosis of central gray matter and adjacent white matter and axonal swelling, whereas spinal cords from group II showed small and localized spinal cord injuries and those from group III revealed no evidence of cord injury. These results indicate that MK-801 and NBQX exert different neuroprotective effects related to different mechanisms of glutamate neurotoxicity mediated by the NMDA receptor and non-NMDA receptor, which initiate a deleterious cascade of biochemical events that ultimately results in delayed-onset paraplegia.
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