The Effective Of Febrile Seizures On The Rat Hippocampal Cam Kinase Ⅱ Phosphorylation Status And Learning And Memory

Hippocampus plays an important role in the nerve injury caused by fibrile seizure(FS).NMDA receptor and CaMKⅡ which are ample in hippocampus regulate synapicplasticity and metaplasticity. How do they act under FS is not clear yet. In thisresearch, FS was induced in10–12-day-old Sprague-Dawley rats using a hair dryer.Until all rats grow up to60days, we use western blot to examine the followings:1.the expression of CaMKⅡ in the rats hippocampus;2. The phosphorylation state ofCaMK Ⅱ; And then the Morris to detect learning and menmory. The resultsdemonstrated that experimental febrile seizures did not result in appreciabledifference in the expression of CaMKⅡ, but it did change the phosphorylation stateof the kinase T305. Three different FS groups show significant difference inT286/T305compare to the control. The Morris Water maze data illustrate the first twodays, the latency of FSⅠgroup and FS Ⅲ group were abvious longer than thecontrol group; Atractively, compare with the control group, the latency of FSⅡ grouphas on difference through four days. Our result show that CaMKⅡ participate in thenever injury caused by FS.