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Journal of ECT:
doi: 10.1097/YCT.0b013e318290f7ff
Original Studies

Effects of Acute and Chronic Electroconvulsive Shocks on Glycogen Synthase Kinase 3β Level and Phosphorylation in Mice

Basar, Koray MD*; Eren-Kocak, Emine MD, PhD*†; Ozdemir, Hatice MD, PhD; Ertugrul, Aygun MD, PhD*†

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Abstract

Objectives

Glycogen synthase kinase 3β (GSK-3β) is recently proposed as a novel target in the treatment of mood disorders. Recent evidence has suggested that acute and chronic administration of antidepressants led to inhibition of GSK-3β via phosphorylation of Serine9 residue. Acute electroconvulsive shock (ECS) has been reported to increase GSK-3β phosphorylation transiently. In this study, the changes in the level of GSK-3β and its phoshorylated form (phospho-Ser9-GSK-3β) following chronic ECS (cECS) were investigated in mice.

Methods

Mice were given daily ECS via bilateral corneal electrodes for 10 consecutive days in the chronic group and a single ECS in the acute group. Electrodes were applied without stimulation in corresponding sham groups. Immunoblotting for GSK-3β and phospho-Ser9-GSK-3β was performed with the frontal cortex and hippocampus samples, extracted 10 minutes after single ECS, and 24 hours after the last ECS in the chronic group. The optical densities of the bands obtained were compared between the active treatment and sham groups for each condition separately.

Results

The level of phospho-Ser9-GSK-3β was not different following chronic ECS, but significantly higher following acute ECS, compared with the corresponding sham group, in the hippocampus and frontal cortex. The level of GSK-3β was similar to sham following both acute and chronic ECS, in both regions.

Conclusions

The transient increase in GSK-3β phosphorylation observed following acute ECS in the mice hippocampus and frontal cortex was not found to persist 24 hours following chronic ECS. The mechanism of action of ECS does not seem to involve persistent change in the level and phosphorylation of GSK-3β.

Copyright © 2013 by Lippincott Williams & Wilkins

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