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central nervous system. , , This suggests that a neuroprotective intervention targeted at enhancing NAAG actions might be particularly well-suited as a therapeutic means of suppressing Glu-mediated excitotoxicity associated with spinal cord injuries or other neuropathological conditions.

Consistent with these expectations, we observed the selective GCP II inhibitor 2-PMPA to significantly reduce post-injury elevation of extracellular Glu and to greatly improve recovery from dynorphin A-induced ischemic spinal cord injury. These data reinforce and extend earlier indications pointing to the potential importance of NAAG and GCP II under pathophysiological circumstances associated with excitotoxic actions of extracellular Glu.

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