Abstract: Objective To study the role of CamkⅡ in acute lead exposure of rathipp ocampus.Methods The hippocampus of 30 day healthy Wistar rat was taken out quickly and cut in to 350μms lices.Afters tabilizing culture for 2 hours in artificial cereb rospinal fluid(ACSF),the slices were diveded in to control(ACSF)group,glutamic acid group,KN 293(CaMKⅡ inhibitor)group and glutamic acid+ lead group.After 30 min culture,the hipp ocampuss lices were collected to detect effects of glutamic acid,KN 293 and lead on extracellular signal regulated kinase2(ERK2).Results Compared with the control group,the re was a 42%ine rease of ERK2 activcty with a significant difference(P<0.05)in glutamic acid guoup.There were a 23% and a 28% decrease of ERK2 activity in KN 293 and lead exposure guoups compared with that of control guoup(P<0.05).Total ERK2 expression was not affected obviously.Conclusion Ac tue lead exposure inhibits CaM KⅡ activity and affects its downs treamsignal resulting in nervous system impairment.