Ryanodine receptors are involved in the improvement of depression-like behaviors through electroconvulsive shock in stressed mice.


Journal

Brain stimulation
ISSN: 1876-4754
Titre abrégé: Brain Stimul
Pays: United States
ID NLM: 101465726

Informations de publication

Date de publication:
Historique:
received: 09 04 2020
revised: 20 10 2020
accepted: 01 11 2020
pubmed: 10 11 2020
medline: 2 10 2021
entrez: 9 11 2020
Statut: ppublish

Résumé

Electroconvulsive therapy (ECT) is effective for treating depression. However, the mechanisms underlying the antidepressant effects of ECT remain unknown. Depressed patients exhibit abnormal Ca We considered that depression may be improved via ECT-induced normalization of intracellular Ca A mouse depression-like model subjected to water immersion with restraint stress was administered electroconvulsive shock (ECS) therapy. Their depression-like status was behaviorally and histologically assessed using forced swimming tests, novelty-suppressed feeding tests, and by evaluating neurogenesis in the hippocampal dentate gyrus, respectively. A RyRs blocker, dantrolene, was administered prior to ECS, and the changes in depression-like conditions were examined. The protein expressions of RyR1 and RyR3 significantly increased in the hippocampus of the mouse model with depression-like symptoms. This increase was attenuated as depression-like symptoms were reduced due to ECS application. However, pre-injection with dantrolene reduced the antidepressant effects of ECS. A significant increase in RyRs expression in a depression-like state and exacerbation of depression-like symptoms by RyRs inhibitors may be caused by RyRs dysfunction, suggesting overexpression of RyRs is a compensatory effect. Normalization of RyRs expression levels by ECS suggests that ECT normalizes the Ca

Sections du résumé

BACKGROUND
Electroconvulsive therapy (ECT) is effective for treating depression. However, the mechanisms underlying the antidepressant effects of ECT remain unknown. Depressed patients exhibit abnormal Ca
OBJECTIVE
We considered that depression may be improved via ECT-induced normalization of intracellular Ca
METHODS
A mouse depression-like model subjected to water immersion with restraint stress was administered electroconvulsive shock (ECS) therapy. Their depression-like status was behaviorally and histologically assessed using forced swimming tests, novelty-suppressed feeding tests, and by evaluating neurogenesis in the hippocampal dentate gyrus, respectively. A RyRs blocker, dantrolene, was administered prior to ECS, and the changes in depression-like conditions were examined.
RESULTS
The protein expressions of RyR1 and RyR3 significantly increased in the hippocampus of the mouse model with depression-like symptoms. This increase was attenuated as depression-like symptoms were reduced due to ECS application. However, pre-injection with dantrolene reduced the antidepressant effects of ECS.
CONCLUSIONS
A significant increase in RyRs expression in a depression-like state and exacerbation of depression-like symptoms by RyRs inhibitors may be caused by RyRs dysfunction, suggesting overexpression of RyRs is a compensatory effect. Normalization of RyRs expression levels by ECS suggests that ECT normalizes the Ca

Identifiants

pubmed: 33166727
pii: S1935-861X(20)30284-9
doi: 10.1016/j.brs.2020.11.001
pii:
doi:

Substances chimiques

Ryanodine Receptor Calcium Release Channel 0
Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

36-47

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest None.

Auteurs

Emi Nakamura-Maruyama (E)

Department of Physiology 2, Kawasaki Medical School, Kurashiki, Japan.

Risa Kai (R)

Department of Physiology 2, Kawasaki Medical School, Kurashiki, Japan.

Naoyuki Himi (N)

Department of Physiology 2, Kawasaki Medical School, Kurashiki, Japan.

Naohiko Okabe (N)

Department of Physiology 2, Kawasaki Medical School, Kurashiki, Japan.

Kazuhiko Narita (K)

Department of Physiology 2, Kawasaki Medical School, Kurashiki, Japan.

Tetsuji Miyazaki (T)

Department of Psychiatry, Kawasaki Medical School, Kurashiki, Japan.

Shozo Aoki (S)

Department of Psychiatry, Kawasaki Medical School, Kurashiki, Japan.

Osamu Miyamoto (O)

Department of Physiology 2, Kawasaki Medical School, Kurashiki, Japan. Electronic address: mosamu@med.kawasaki-m.ac.jp.

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Classifications MeSH