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Article: Rotarod training reverses corticosterone-induced motor deficits via oligodendrocyte lineage cell modulation

TitleRotarod training reverses corticosterone-induced motor deficits via oligodendrocyte lineage cell modulation
Authors
Issue Date5-Jul-2025
PublisherMedknow Publications
Citation
Neural Regeneration Research, 2025 How to Cite?
Abstract

Adult-born oligodendrocytes are continuously produced in the brains of rodents. The functional role of these cells has been linked to the motor-related activities of healthy animals and is vital for acquiring new motor skills. However, the relationship between these cells and the control of motor-related activities has not been investigated in pathological conditions. Therefore, the aim of this study is to investigate the role of oligodendrocytes in depression-related motor deficits and the effects of training. Psychomotor retardation is a key symptom of depression. Consistent with the impairments observed in rodent motor performance, the proliferation and activation of adult-born oligodendrocytes are altered in a corticosterone-induced stress paradigm. Therapeutic rotarod training can alleviate these symptoms by reversing the aforementioned changes. Notably, these alterations are particularly pronounced in layer I of the motor cortex. Thus, this study provides evidence of the potential functional involvement of adult-born oligodendrocytes in the motor impairments observed in the depressed animals. Additionally, it offers preliminary results for further investigation into layer I of the motor cortex in relation to these pathological conditions.


Persistent Identifierhttp://hdl.handle.net/10722/366535
ISSN
2023 Impact Factor: 5.9
2023 SCImago Journal Rankings: 0.967

 

DC FieldValueLanguage
dc.contributor.authorLee, Jada Chia-Di-
dc.contributor.authorLau, Benson Wui-Man-
dc.contributor.authorYau, Suk-Yu-
dc.contributor.authorLeung, Wai-Hin Joseph-
dc.contributor.authorWong, Harmony Kai-Hei-
dc.contributor.authorVidana, Dalinda Isabel Sanchez-
dc.contributor.authorLee, Tatia M.C.-
dc.contributor.authorWu, Wu-Tian-
dc.contributor.authorSo, Kwok-Fai-
dc.date.accessioned2025-11-25T04:19:57Z-
dc.date.available2025-11-25T04:19:57Z-
dc.date.issued2025-07-05-
dc.identifier.citationNeural Regeneration Research, 2025-
dc.identifier.issn1673-5374-
dc.identifier.urihttp://hdl.handle.net/10722/366535-
dc.description.abstract<p>Adult-born oligodendrocytes are continuously produced in the brains of rodents. The functional role of these cells has been linked to the motor-related activities of healthy animals and is vital for acquiring new motor skills. However, the relationship between these cells and the control of motor-related activities has not been investigated in pathological conditions. Therefore, the aim of this study is to investigate the role of oligodendrocytes in depression-related motor deficits and the effects of training. Psychomotor retardation is a key symptom of depression. Consistent with the impairments observed in rodent motor performance, the proliferation and activation of adult-born oligodendrocytes are altered in a corticosterone-induced stress paradigm. Therapeutic rotarod training can alleviate these symptoms by reversing the aforementioned changes. Notably, these alterations are particularly pronounced in layer I of the motor cortex. Thus, this study provides evidence of the potential functional involvement of adult-born oligodendrocytes in the motor impairments observed in the depressed animals. Additionally, it offers preliminary results for further investigation into layer I of the motor cortex in relation to these pathological conditions.<br></p>-
dc.languageeng-
dc.publisherMedknow Publications-
dc.relation.ispartofNeural Regeneration Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleRotarod training reverses corticosterone-induced motor deficits via oligodendrocyte lineage cell modulation-
dc.typeArticle-
dc.identifier.doi10.4103/NRR.NRR-D-24-00448-
dc.identifier.eissn1876-7958-
dc.identifier.issnl1673-5374-

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