AUTHOR(S): Hiroshi Kadotani, Shobu Namura, Goro Katsuura, Toyoaki Terashim, Haruhiko Kikuchi
ABSTRACT: 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 receptor attenuates focal cerebral ischemic injury after permanent MCA occlusion, and that a low level of NR2C is expressed and active in the cerebral cortex. NR2-C deficient mice do not show impairement of motor coordination or motor learning. Therefore the development of drugs selectively inhibiting NR2C may prove beneficial in the treatment of stroke and traumatic brain injuries.
KEYWORDS: NMDA receptor, Mutant mice, Gene knockout, Cerebral infarction, MCA occlusion, Ischemic brain injury, Stroke, Binding assay
SUBJECT TITLE: NR2C and cerebral ischemia