<正>Objective: To investigate the activation （phosphorylation） and subcellular localization of extracellular signal-regulated kinase （ERK1/2）. as well as the possible mechanism

following cerebral ischemia and ischemia/reperfusion in rat hippocampus. Methods: Transient brain ischemia was induced by the four-vessel occlusion method in Sprague-Dawley rats. Western blot analysis. Results: During cerebral ischemia without reperfusion ERK1/2 activation immediately increased with a peak at 5 min and then decreased in the cytosol fraction

which was paralleled by the increase of ERK1/2 activation in the nucleus fraction. During reperfusion

ERK1/2 was activated with peaks occurring at 10 min in the cytosol and at 30 min in the nucleus

respectively. Under those conditions

the protein expressions had no significant change. In order to clarify the possible mechanism of ERKl/2 activation

the rats were intraperitoneally administrated with N-methyl-D-aspartate （NMDA） receptor antagonist dextromethorphan（DM）

L-type voltage-gated Ca2+ channel （L-VGCC） antagonist nifedipine （ND） 20 min before ischemia

finding that DM and ND markedly prevented ERKl/2 activation of nucleus fraction induced by reperfusion. not by ischemia. Conclusion: These results suggested that the nuclear translocation mainly occurred during ischemia

while ischemia-reperfusion induced ERK1/2 activation both in the cytosol and the nucleus. Two type calcium channels contributed

at least partially

to the activation of ERK1/2.