Role of Dopamine D2 Receptor in Stress-Induced Myelin Loss
- Authors
- Choi, Mi-Hyun; Na, Ji Eun; Yoon, Ye Ran; Lee, Hyo Jin; Yoon, Sehyoun; Rhyu, Im Joo; Baik, Ja-Hyun
- Issue Date
- 14-9월-2017
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- SCIENTIFIC REPORTS, v.7
- Indexed
- SCIE
SCOPUS
- Journal Title
- SCIENTIFIC REPORTS
- Volume
- 7
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/82239
- DOI
- 10.1038/s41598-017-10173-9
- ISSN
- 2045-2322
- Abstract
- Dopaminergic systems play a major role in reward-related behavior and dysregulation of dopamine (DA) systems can cause several mental disorders, including depression. We previously reported that dopamine D2 receptor knockout (D2R(-/-)) mice display increased anxiety and depression-like behaviors upon chronic stress. Here, we observed that chronic stress caused myelin loss in wild-type (WT) mice, while the myelin level in D2R(-/-) mice, which was already lower than that in WT mice, was not affected upon stress. Fewer mature oligodendrocytes (OLs) were observed in the corpus callosum of stressed WT mice, while in D2R(-/-) mice, both the control and stressed group displayed a decrease in the number of mature OLs. We observed a decrease in the number of active beta-catenin (ABC)-expressing and TCF4-expressing cells among OL lineage cells in the corpus callosum of stressed WT mice, while such regulation was not found in D2R(-/-) mice. Administration of lithium normalized the behavioral impairments and myelin damage induced by chronic stress in WT mice, and restored the number of ABC-positive and TCF4-positive OLs, while such effect was not found in D2R(-/-) mice. Together, our findings indicate that chronic stress induces myelin loss through the Wnt/beta-catenin signaling pathway in association with DA signaling through D2R.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- Graduate School > Department of Life Sciences > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.