ATTENUATION OF FOCAL CEREBRAL INFARCT IN MICE LACKING NMDA RECEPTOR SUBUNIT NR2C

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.