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Hypothermia inhibits translocation of CaM kinase II and PKC‐α, β, γ isoforms and fodrin proteolysis in rat brain synaptosome during ischemia‐reperfusion
Author(s) -
Harada Kazuki,
Maekawa Tsuyoshi,
Tsuruta Ryosuke,
Kaneko Tadashi,
Sadamitsu Daikai,
Yamashima Tetsumori,
Yoshida Kenichi
Publication year - 2002
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.10159
Subject(s) - calpain , protein kinase c , ischemia , hypothermia , synaptosome , gene isoform , chromosomal translocation , kinase , proteolysis , brain ischemia , pharmacology , microbiology and biotechnology , biology , chemistry , medicine , biochemistry , endocrinology , enzyme , central nervous system , gene
To clarify the involvement of intracellular signaling pathway and calpain in the brain injury and its protection by mild hypothermia, immunoblotting analyses were performed in the rat brain after global forebrain ischemia and reperfusion. After 30 min of ischemia followed by 60 min of reperfusion, Ca 2+ /calmodulin‐dependent kinase II (CaM kinase II) and protein kinase C (PKC)‐α, β, γ isoforms translocated to the synaptosomal fraction, while mild hypothermia (32°C) inhibited the translocation. The hypothermia also inhibited fodrin proteolysis caused by ischemia‐reperfusion, indicating the inhibition of calpain. These effects of hypothermia may explain the mechanism of the protection against brain ischemia‐reperfusion injury through modulating synaptosomal function. © 2002 Wiley‐Liss, Inc.