Extracellular signal-regulated kinase 1/2 activation in hippocampus after cerebral ischemia may not interfere with postischemic cell death

To investigate the effect of the activation of extracellular signal-regulat ed kinase 112 (ERK1/2) on cerebral ischemic injury, temporospatial alterati ons of active (diphosphorylated) ERK1/2 immunoreactivity in hippocampus was examined. Western blot showed that diphosphorylated ERK1/2 were decreased at 10 min of cerebral ischemia but increased rapidly (within 2 min) and tra nsiently (within 4 h) during reperfusion. Immunohistochemistry showed that little diphosphorylated ERK1/2 immunoreactivity was seen in CA1 pyramidal c ell bodies after ischemia. while strong immunoreactivity were seen in neuro nal bodies in CA3/DG and in fiber systems in both CA1 and CA3 regions. Cere bral ventricular infusion of PD98059, a specific inhibitor of ERK kinase, c ompletely prevented ERK1/2 activation after ischemia but had no effect on t he survival of pyramidal cells in CA1 subfield. The results suggest that ER K 112 activation in hippocampus after brain ischemia may not interfere with the postischemic cell death in CA1 region. (C) 2001 Elsevier Science B.V. All rights reserved.