Journal
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
Volume 64, Issue -, Pages 320-324Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pnpbp.2015.03.010
Keywords
Antidepressant; Brain-derived neurotrophic factor (BDNF); Depression; Histone deacetylase; Histone deacetylase (HDAC) inhibitor
Funding
- Ministry of Education, Science, and Culture of Japan [23659566, 25116518]
- Ministry of Health and Welfare of Japan
- Core Research for Evolutional Science and Technology (CREST)
- Japan Science and Technology Agency (JST)
- Ministry of Education, Culture, Sports, Science and Technology (MEXT)
- Grants-in-Aid for Scientific Research [25116518, 15K19731, 23659566] Funding Source: KAKEN
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Numerous preclinical studies demonstrate that changes in gene expression in the brain occur in animal models of depression using exposure to stress, such as social defeat and leaned helplessness, and that repeated administration of antidepressants ameliorates these stress-induced changes in gene expression. These findings suggest that alteration in gene transcription in the central nervous system in response to stress plays an important role in the pathophysiology of depression. Recent advances in epigenetics have led to the realization that chromatin remodeling mediated by histone deacetylase (HDAC) is closely involved in the regulation of gene transcription. In this context, we first review several preclinical studies demonstrating the antidepressant-like efficacy of HDAC inhibitors. We then suggest the efficacy of HDAC inhibitors in treatment-resistant depression based on the mechanism of action of HDAC. Finally, we discuss the possibility of using HDAC inhibitors in patients with treatment-resistant depression. (C) 2015 Elsevier Inc. All rights reserved.
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