BACKGROUND: Massive release of glutamate plays an important role in ischemic neuronal injury, and modification of this process may provide neuroprotection. We studied the protective effects of the N- methyl-D-aspartate receptor antagonist ketamine on hind limb motor function and glutamate receptor of gene expression in an experimental model of spinal cord ischemia. METHODS: Transient spinal cord ischemia was induced by 15 min of thoracic aortic occlusion in 24 anesthetized Sprague-Dawly rats. Rats were randomly assigned to one of three treatment groups (n = 8 each): C group, no intervention; K30 group, ketamine 30 mg/kg intravenously; or K50 group, ketamine 50 mg/kg intravenously. Normothermia (38degreesC) was maintained during ischemia. After spinal ischemia neurologic function was evaluated immediately and after 1, 2 and 3 hours. After 3 hours rats were euthanized and spinal cords were removed for the assay of NMDAR and mGluR5 mRNA. RESULTS: Neurologic outcome was better in the K30 group than the C or K50 group (P < 0.05). The NMDAR mRNA expression of the K30 and K50 group were greater than those of the C group. The mGluR5 mRNA expression increased after spinal ischemia. There were no differences between groups. CONCLUSIONS: In this study demonstrated that treatment with ketamine 30 mg/kg intravenously before ischemia increases tolerance of spinal cord motor neurons in a period of normothermic ischemia.