Spinal Cord Injury by Transient Ischemia is Reduced in Mice Deficient in the ε 1 (NR2A) Subunit of NMDA Receptor Channel

The role of glutamate neurotoxicity in spinal cord has been advocated but still remains controversial. In spinal cord, as well as other central nervous system tissues, glutamate receptors are thought to participate in neuronal cell death by transient ischemia, but it is not clear which subtype of glutamate receptor cannels acts in the mechanism of excitotoxicity. To elucidate the involvement of glutamate receptors, especially NMDA receptors, in spinal cord ischemic injury, we used mutant mice deficient in the ε 1 (NR 2 A) subunit of NMDA receptor. The mutant mice were subjected to transient spinal cord ischemia by clamping aortic arch and left subclavian artery and examined for 48 hours after ischemia. Their motor dysfunction and histopathological damage were significantly milder compared with wild type mice. These results indicate that NMDA receptors which contain ε 1 subunit play important role in the mechanism of neurotoxicity in spinal cord