Effects of propofol and dizocilpine maleate on the cognitive abilities and the hyperphosphorylation of Tau protein of rats after the electroconvulsive therapy.
- Author:
Chao LIU
1
;
Su MIN
;
Ke WEI
;
Dong LIU
;
Jun DONG
;
Jie LUO
;
Ping LI
;
Xiao-bin LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Depression; metabolism; psychology; Disease Models, Animal; Dizocilpine Maleate; pharmacology; Electroconvulsive Therapy; Glutamic Acid; metabolism; Hippocampus; drug effects; metabolism; Male; Maze Learning; drug effects; Memory; drug effects; Phosphorylation; drug effects; Propofol; pharmacology; Rats; Rats, Sprague-Dawley; tau Proteins; metabolism
- From: Acta Academiae Medicinae Sinicae 2012;34(4):324-329
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo explore the effects of propofol and dizocilpine maleate (MK-801) on the cognitive abilities the hyperphosphorylation of Tau protein of rats after the electroconvulsive therapy.
METHODSTwo intervention factors including electroconvulsive shock therapy (ECT) (two levels: not applied and one treatment course) and drug intervention (three levels: intravenous saline,intravenous MK-801, and intravenous propofol). The morris water maze test started within 1 day after ECT to evaluate the learning-memory. The glutamate level in the hippocampus of rats was determined by high-performance liquid chromatography. The Tau protein that includes Tau5 (total Tau protein), PHF-1 (pSer(396/404)), AT8 (pSer(199/202)), and 12E8 (pSer(262)) in the hippocampus of rats was determined using Western blotting.
RESULTSPropofol, MK-801, and ECT could induce the impairment of learning-memory in depressed rats. The electroconvulsive shock significantly up-regulated the glutamate level, which was reduces by the propofol. The ECT up-regulated the hyperphosphorylation of Tau protein in the hippocampus of depressed rats, which was reduced by propofol and MK-801.
CONCLUSIONBoth propofol and MK-801 could protect against the impairment of learning-memory and reduce the hyperphosphorylation of Tau protein induced by ECT in depressed rats.
