한빛사논문
- 조회1,355
Jin-Seok Lee1, Sung-Bae Lee1, Dong-Woon Kim2, Nara Shin2, Seon-Ju Jeong3, Chae-Ha Yang3, Chang-Gue Son1,*
1Institute of Bioscience & Integrative Medicine, Dunsan Hospital of Daejeon University, Daejeon, Republic of Korea. 2Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, Republic of Korea. 3Department of Physiology, College of Korean Medicine, Daegu Haany Uni-versity, Daegu, Republic of Korea.
*Corresponding author.
Abstract
Social isolation is common in modern society and is a contributor to depressive disorders. People with depression are highly vulnerable to alcohol use, and abusive alcohol consumption is a well-known obstacle to treating depressive disorders. Using a mouse model involving isolation stress (IS) and/or ethanol intake, we investigated the mutual influence between IS-derived depressive and ethanol-seeking behaviors along with the underlying mechanisms. IS increased ethanol craving, which robustly exacerbated depressive-like behaviors. Ethanol intake activated the mesolimbic dopaminergic system, as evidenced by dopamine/tyrosine hydroxylase double-positive signals in the ventral tegmental area and c-Fos activity in the nucleus accumbens. IS-induced ethanol intake also reduced serotonergic activity, via microglial hyperactivation in raphe nuclei, that was notably attenuated by a microglial inhibitor (minocycline). Our study demonstrated that microglial activation is a key mediator in the vicious cycle between depression and alcohol consumption. We also propose that dopaminergic reward might be involved in this pathogenicity.
논문정보
- Research article
- 2021년 11월 (BRIC 등록일 2021-11-12)
- 국내 연구진
- 의약학 > 한의학
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