The Journal of ECT

Skip Navigation LinksHome > December 2012 - Volume 28 - Issue 4 > Effects of Propofol on the Activation of Hippocampal CaMKIIα...
Journal of ECT:
doi: 10.1097/YCT.0b013e31826140c7
Original Studies

Effects of Propofol on the Activation of Hippocampal CaMKIIα in Depressed Rats Receiving Electroconvulsive Therapy

Li, Xiao MSm; Li, Wei MD; Luo, Jie MD; Wei, Ke MD; Li, Ping MD; Liu, Xiao-bin MSm; Min, Su BSm

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Objectives: The aim of this study was to investigate the effects of propofol on the activation of hippocampal calcium/calmodulin-dependent protein kinase IIα (CaMKIIα) in electroconvulsive therapy (ECT) in a rat model of depression.

Methods: Sprague-Dawley rats were stressed repeatedly for 28 days to establish a depressed model. Forty depressed rats were then randomly assigned (n = 10 per group) to the depression group, propofol group (received propofol once a day for 1 week), ECT group (treated with ECT once a day for 1 week), or propofol + ECT group (treated with ECT pretreated and propofol once a day for 1 week). Their depressive state was assessed using the sucrose preference test and open-field test, whereas their learning and memory were evaluated using the Morris water maze task. The expression levels of CaMKIIα and phosphorylated CaMKIIα (pCaMKIIα) were detected by immunohistochemistry.

Results: Compared with the depression group, the ECT and propofol + ECT groups had higher sucrose preference percentages and scored higher on the open-field test. The ECT group exhibited longer escape latency, shorter space exploration time, down-regulated expressions of CaMKIIα and pCaMKIIα in the hippocampus, and lower pCaMKIIα/CaMKIIα values. The propofol + ECT group showed up-regulated expressions of CaMKIIα and pCaMKIIα in the hippocampus. Compared with the ECT group, the propofol + ECT group exhibited shorter escape latency, longer space exploration time, up-regulated expressions of CaMKIIα and pCaMKIIα, and higher pCaMKIIα/CaMKIIα values.

Conclusions: Propofol may potentially alleviate ECT-induced learning/memory impairment in depressed rats by enhancing CaMKIIα activation in the hippocampus.

© 2012 Lippincott Williams & Wilkins, Inc.


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