• Wei-ran Liu and Yun Yue.
• Department of Anesthesiology, Cancer Institute & Hospital, Tianjin Medical University, Tianjin 300060, China.
• Zhonghua Yi Xue Za Zhi. 2012 Aug 21; 92 (31): 2210-3.

ObjectiveTo examine whether the isoflurane-induced spatial memory changes is associated with AD pathogenesis of tau protein phosphorylation.MethodsWe exposed 18-month-old male Sprague-Dawley rats to 1.4% isoflurane for 2 hours (anesthesia group, n = 31). Spatial memory was measured with the Morris water maze before and 2 days after anesthesia. Behavioral testing of the training group (n = 20), without anesthetics, was performed currently with the anesthesia group. The control group (n = 10) received no anesthesia or behavioral testing. We calculated the average escape latency of every training day for each rat. We divided the anesthesia group into an isoflurane-induced severe memory impairment group (SIG) and a no severe memory impairment group (NSIG) according to whether prolonged escape latency of each day after anesthesia was more than 1.96 SD of mean escape latency for the training group. Following behavioral testing, total tau protein (T-Tau), p-Tau-Thr231 (pT231), p-Tau-Ser396 (pS396), glycogen synthase kinase 3β (GSK-3β) and protein phosphatase 2A (PP2A) were quantified by Western blot.ResultsSix rats had severe post-anesthesia impairments. The expressions of T-Tau, pT231, pS396, GSK-3β and PP2A in the SIG exhibited no differences as compared with the NSIG, training and control groups.ConclusionTau protein phosphorylation in hippocampus may be irrelevant for isoflurane-induced spatial memory impairment in senile rats.

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