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Sleep and Circuit Plasticity

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Front. Neural Circuits | doi: 10.3389/fncir.2018.00014

Sleep Deprivation and the Epigenome

  • 1Department of Molecular Physiology and Biophysics, University of Iowa, United States

Sleep deprivation disrupts the lives of millions of people every day and has a profound impact on the molecular biology of the brain. These effects begin as changes within a neuron, at the DNA and RNA level, and result in alterations in neuronal plasticity and dysregulation of many cognitive functions including learning and memory. The epigenome plays a critical role in regulating gene expression in the context of memory storage. In this review, we begin by describing the effects of epigenetic alterations on the regulation of gene expression, focusing on the most common epigenetic mechanisms: (i) DNA methylation, (ii) histone modifications, and (iii) non-coding RNAs. We then discuss evidence suggesting that sleep loss impacts the epigenome and that these epigenetic alterations might mediate the changes in cognition seen following disruption of sleep. The link between sleep and the epigenome is only beginning to be elucidated, but clear evidence exists that epigenetic alterations occur following sleep deprivation. In the future, these changes to the epigenome could be utilized as biomarkers of sleep loss or as therapeutic targets for sleep-related disorders.

Keywords: Sleep Deprivation, DNA Methylation, Histone Modifications, MicroRNAs, Long non-coding RNA (lncRNA)

Received: 04 Aug 2017; Accepted: 29 Jan 2018.

Edited by:

Paul J. Shaw, School of Medicine, Washington University in St. Louis, United States

Reviewed by:

Sushil K. Jha, Jawaharlal Nehru University, India
Matthew Thimgan, Missouri University of Science and Technology, United States  

Copyright: © 2018 Gaine, Chatterjee and Abel. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Ted Abel, University of Iowa, Department of Molecular Physiology and Biophysics, Iowa City, Iowa, United States,