Harada Kazuki, Maekawa Tsuyoshi, Tsuruta Ryosuke, Kaneko Tadashi, Sadamitsu Daikai, Yamashima Tetsumori, Yoshida Ki Ken-ichi
Department of Emergency and Critical Care Medicine, Yamaguchi University School of Medicine, Yamaguchi, Japan.
J Neurosci Res. 2002 Mar 1;67(5):664-9. doi: 10.1002/jnr.10159.
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, Ca2+/calmodulin-dependent kinase II (CaM kinase II) and protein kinase C (PKC)-alpha, beta, gamma isoforms translocated to the synaptosomal fraction, while mild hypothermia (32 degrees 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.