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Delayed induction of αB‐crystallin in activated glia cells of hippocampus in kainic acid‐treated mouse brain
Author(s) -
Che Yongzhe,
Piao Chun Shu,
Han PyungLim,
Lee JaKyeong
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1170
Subject(s) - kainic acid , hippocampus , hsp27 , heat shock protein , gliosis , hsp70 , biology , psychological repression , chemistry , neuroscience , medicine , endocrinology , microbiology and biotechnology , biochemistry , glutamate receptor , gene expression , receptor , gene
Abstract Small heat shock proteins have been implicated in playing a role in various cellular processes, including stress‐induced cell death. In kainic acid (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 αB‐crystallin, a member of the small heat‐shock protein family, was strongly induced in reactive astrocytes in hippocampus after KA‐induced seizure. The induction was localized mainly in the CA3 region of hippocampus, where massive neuronal loss occurred. We also demonstrated that the delayed induction of αB‐crystallin and HSP27 immunoreactivities in the hippocampus of epileptic animals was repressed to the levels seen in control animals with preadministration of the selective nNOS inhibitor 7‐nitroindazole (7‐NI). This repression was reversed by coinjection of L‐arginine, a substrate of NOS. Together, these data suggest a role for αB‐crystallin and HSP27 in reactive gliosis and/or in delayed neuronal death proceeded after KA‐induced seizure. J. Neurosci. Res. 65:425–431, 2001. © 2001 Wiley‐Liss, Inc.