NEURONAL death following cerebral vascular occlusion may be caused in
part by the action of glutamate acting through the NMDA receptor. Here
we demonstrate that gene disruption of the NR2C subunit of the NMDA r
eceptor attenuates focal cerebral ischemic injury after permanent MCA
occlusion, and that a low level of NR2C is expressed and active in the
cerebral cortex. NR2C-deficient mice do not show impairment of motor
coordination or motor learning. Therefore the development of drugs sel
ectively inhibiting NR2C may prove beneficial in the treatment of stro
ke and traumatic brain injuries. (C) 1998 Rapid Science Ltd.