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Electroconvulsive Shock Increases SIRT1 Immunoreactivity in the Mouse Hippocampus and Hypothalamus

Chung, Sung BS*; Kim, Hee Jeong BS*; Yoon, In Seon BS*; Kim, Hyun Ju PhD*; Choi, Sun Hye MS*; Kim, Yong Sik MD, PhD; Shin, Kyung Ho MD, PhD*

doi: 10.1097/YCT.0b013e31827659f7
Original Studies

Objectives Recent study shows that silent mating-type information regulation 2 homolog 1 (SIRT1) regulation may be involved with depression. Electroconvulsive shock (ECS) has been used for the treatment of depression, but little is known about the effect of ECS on the changes in SIRT1 levels in the brain. The present study was designed to observe whether ECS dynamically regulates SIRT1 levels in the hippocampus and hypothalamus; both of these regions have been implicated in the pathophysiology of depression.

Methods Male imprinting control region mice were given a single ECS via ear clip electrodes, and then killed 0.5, 2, 8, 24, or 48 hours after ECS. Changes in SIRT1 were observed by Immunohistochemistry, and obtained results were compared with sham controls that did not receive ECS.

Results Silent mating-type information regulation 2 homolog 1 immunoreactivity levels in the CA1 and CA3 subfields of the hippocampus peaked 2 hours after ECS and then returned to control levels by 24 hours after ECS. Silent mating-type information regulation 2 homolog 1 immunoreactivity levels in the dentate gyrus of hippocampus, hypothalamic paraventricular, dorsomedial, arcuate, and suprachiasmatic nuclei peaked 8 hours after ECS but had not completely returned to baseline levels 48 hours after ECS, except for the dentate gyrus. Electroconvulsive shock resulted in a gradual increase of SIRT1 immunoreactivity in the hypothalamic ventromedial nucleus and lateral hypothalamic area, which appeared to be still rising or peaking at the 48-hour post-ECS time point.

Conclusions The present results demonstrate that a single ECS increases SIRT1 in the mouse hippocampus and hypothalamus differentially in a region-specific time-dependent manner.

Supplemental digital content is available in the text.

From the *Department of Pharmacology, Korea University College of Medicine, Anam-Dong, Sungbuk-Gu, Seoul, Republic of Korea and †Department of Psychiatry and Behavioral Science, Seoul National University College of Medicine, Seoul, Republic of Korea.

Received for publication June 7, 2012; accepted September 26, 2012.

Reprints: Kyung Ho Shin, MD, PhD, Department of Pharmacology, Korea University College of Medicine, 126-1, 5-ga, Anam-dong, Sungbuk-gu, Seoul 136-705, Republic of Korea (e-mail:

The authors have no conflicts of interest or financial disclosures to report.

This study was supported by grants of the Korea Health 21 R&D project, Ministry for Health, Welfare and Family Affairs (A030001) and the National Research Foundation of Korea (R1009842) funded by the Korean government.

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© 2013 by Lippincott Williams & Wilkins