INDUCTION OF aB-CRYSTALLIN IN ACTIVATED ASTROCYTES OF HIPPOCAMPUS IN KA-TREATED MOUSE BRAINX

초록

Small heat shock proteins have been implicated to play a role in various cellular processes including stress-induced cell death. In KA-treated rat brain, the immunoreactivity of heat shock protein 27 (HSP27) was markedly increased in glia cells of the limbic system. In the present study, we demonstrated that aB-crystallin, a member of small heat shock protein family, was strongly induced in reactive astrocytes in the hippocampus after KA-induced seizure. The induction was detected 3-4 days after KA-treatment and localized mainly in the CA3 region of hippocampus, where a massive neuronal loss underwent. The induction of aB crystalline was sustained for up to 10 days after the KA-treatment. We also demonstrated that the delayed induction of aB-crystalline and hsp27 immunoreactivities in the hippocampus of epileptic animals was repressed to the levels seen in control animals by pre-administration of selective nNOS inhibitor, 7-nitroindazole (7-NI), which was accompanied by the suppression of delayed neuronal death in hippocampus. Such a repression was reversed by the co-injection of L-arginine, a substrate of NOS, that was coincided with the aggravation of neuronal death. Together, these data suggest a role of αB-crystallin in reactive gliosis and/or in delayed neuronal death proceeded after KA-induced seizure