c-Jun N-terminal kinase activation in hippocampal CAI region was involved in ischemic injury

To clarify the role of c-Jun N-terminal kinase (JNK) activation in brain is chemia, temporospatial alteration of active (diphosphorylated) JNK1/2 immun oreactivity in hippocampus after brain ischemia in rat was investigated. We stern immunoblot study showed that JNK1/2 diphosphorylation level was incre ased biphasically in CA1 but not CA3/dentate gyrus (DG) after 10 min of isc hemia. Cerebral ventricular infusion of JNK1/2 antisense oligonucleotides n ot only significantly decreased JNK1/2 protein expression and the activatio n level but also significantly decreased CA1 pyramidal cell death (demonstr ated by cresyl violet staining) and DNA fragmentation (demonstrated by in s itu end-labeling of DNA). These results suggest that JNK1/2 were selectivel y activated and involved in the selective cell death in hippocampal CA1 sub field after cerebral ischemia. NeuroReport 12:897-900 (C) 2001 Lippincott W illiams & Wilkins.