Introduction:Antipsychotic drugs (APDs) are the first-line pharmacological treatments for schizophrenia. Recent human studies have found that myelin integrity could be improved by APD treatment in schizophrenia patients. Previous studies indicated that regulation of oligodendrocyte development and function may be a novel target for APDs.Aims:The aim of this current study was to examine the possible effects of the antipsychotic drugs (APDs) haloperidol (HAL), olanzapine (OLA), and quetiapine (QUE) on the development of oligodendroglial lineage cells.Main methods:CG4 cells, an oligodendrocyte progenitor cell line, were treated with various concentrations of HAL, OLA, or QUE for specific periods. The proliferation and differentiation of the CG4 cells were measured. The regulation of CG4 cell differentiation by oligodendrocyte lineage transcription factors 1 and 2 (Olig1 and Olig2) was examined.Results:The APDs used in this study had no effect on the proliferation of CG4 cells. The APDs elevated the expression of 2’,3’-cyclic nucleotide 3’-phosphodiesterase (CNP), a specific marker of oligodendrocytes, and promoted the CG4 cells to differentiate into CNP positive oligodendrocytes. QUE and OLA increased the expression of Olig1 and Olig2 whereas HAL only increased the expression of Olig2.Conclusions:Our findings suggest that oligodendrocyte development is a target of HAL, OLA, and QUE and provide further evidence of the important role of oligodendrocytes in the pathophysiology and treatment of schizophrenia. They also indicate that the expression level of oligodendrocyte/myelinrelated genes could be profoundly affected by APDs.
Deep-brain magnetic stimulation (DMS) is an effective therapy for various neuropsychiatric disorders including major depression disorder. The molecular and cellular mechanisms underlying the impacts of DMS on the brain remain unclear. Studies have reported abnormalities in the white matter of depressive brains, suggesting the involvement of myelin and oligodendrocyte pathologies in the development of major depressive disorder. In this study, we use a cuprizone induced demyelination animal model to generate depressive like behaviours and white matter and oligodendrocyte damages. Meanwhile, we treated the animal with DMS 20 minutes daily during the cuprizone challenge or recovery period. Behavioural tests, including nesting, new objective recognition, working memory and depression-like behaviours were tested periodically. Histological staining and western blotting were used to examine the underlying mechanism of DMS. We found that DMS reverse cuprizone induced behavioural deficits in acute demyelination but not during the recovery period. DMS alleviated demyelination and inflammation induced by cuprizone. During the recovery period, DMS had no impacts on overall neural progenitor cell proliferation, but enhanced the maturation of oligodendrocyte. This data suggest that DMS may be a promising treatment option for improving white matter function in psychiatric disorders and neurological diseases in future.Disclosure of interestThe authors have not supplied their declaration of competing interest.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.