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Updated: May 16, 2026
Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
Published on: March 22, 2016
[Correlation of cognitive impairment and Tau protein phosphorylation after isoflurane exposure in senile rats]
1Department of Anesthesiology, Cancer Institute & Hospital, Tianjin Medical University, Tianjin 300060, China.
Objective:
To examine whether the isoflurane-induced spatial memory changes is associated with AD pathogenesis of tau protein phosphorylation.
Methods:
We 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.
Results:
Six 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.
Conclusion:
Tau protein phosphorylation in hippocampus may be irrelevant for isoflurane-induced spatial memory impairment in senile rats.
