• Xue-Sheng Liu, Qing-sheng Xue, Qing-Wen Zeng, Qian Li, Jian Liu, Xiao-Mei Feng, and Bu-Wei Yu.
• Department of Anesthesiology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, PR China.
• Neurobiol Learn Mem. 2010 Nov 1;94(4):461-7.

AbstractSevoflurane administration impairs memory processes in both humans and animals. Increasing evidence suggests that enhancement of the phosphorylation state of glycogen synthase kinase-3β (GSK-3β), as a result of acute administration of lithium chloride (LiCl), may enhance memory consolidation. The current experiments examined whether GSK-3β phosphorylation was involved in mediating the memory impairing effects of posttraining sevoflurane on inhibitory avoidance (IA) retention. In experiment 1, adult male Sprague-Dawley rats were exposed to sevoflurane (0.5%, 1%, or 2%) for 2h immediately after training in a continuous multiple-trail IA paradigm. Sevoflurane (2% inspired) induced significant impairment of retention performance on a 24-h test and inhibited phosphorylation of GSK-3β in the hippocampus 2h after training. In experiment 2, administration of LiCl (100mg/kg, intraperitoneally) 30 min before IA training not only blocked the sevoflurane-induced impairment of consolidation, but also reversed the inhibitory effect of sevoflurane on GSK-3β phosphorylation in the hippocampus. Collectively, these findings support the hypothesis that sevoflurane exposure can impair consolidation of IA memory in rats. Sevoflurane-induced amnesia may be due, at least in part, to suppression of GSK-3β phosphorylation in the hippocampus.Copyright © 2010 Elsevier Inc. All rights reserved.

31 keywords...

hide…