Methylation, memory and addiction

Bali, Purva; Im, Heh‐In; Kenny, Paul J.

doi:10.4161/epi.6.6.15905

Cited by 28 publications

(17 citation statements)

References 38 publications

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“…DNMT1 and DNMT3A seem to mediate activity-dependent methylation in the adult brain 118 , whereas ten-eleven translocase 1 (TET1) and TET3 have crucial roles in activity-dependent demethylation 119,121 . Following these initial studies, DNA methylation has been shown to have a regulatory role in a variety of plasticity-related behaviours, including reward learning 122 , drug addiction 123 and adaptations to stress 124 .…”

Section: Figurementioning

confidence: 99%

The landscape of DNA methylation amid a perfect storm of autism aetiologies

2016

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Increasing evidence points to a complex interplay between genes and the environment in autism spectrum disorder (ASD), including rare de novo mutations in chromatin genes such as methyl-CpG binding protein 2 (MECP2) in Rett syndrome. Epigenetic mechanisms such as DNA methylation act at this interface, reflecting the plasticity in metabolic and neurodevelopmentally regulated gene pathways. Genome-wide studies of gene sequences, gene pathways and DNA methylation are providing valuable mechanistic insights into ASD. The dynamic developmental landscape of DNA methylation is vulnerable to numerous genetic and environmental insults: therefore, understanding pathways that are central to this ‘perfect storm’ will be crucial to improving the diagnosis and treatment of ASD.

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Section: Figurementioning

confidence: 99%

The landscape of DNA methylation amid a perfect storm of autism aetiologies

2016

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“…Environmental toxins, medications, diet, and psychological stress alter epigenetic processes such as DNA methylation, covalent histone modification (e.g., acetylation and methylation), and non-coding RNA expression. Accumulating evidence demonstrates that these processes play an important role in synaptic plasticity during memory formation as epigenetic changes correlate with hippocampal activity [5–10]. Given that peripheral and central sensitization under chronic pain conditions share common mechanisms with the neuronal plasticity of memory formation, it is very likely that similar epigenetic mechanisms occur under both conditions.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic Regulation of Chronic Pain

et al. 2015

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Chronic pain arising from peripheral inflammation and tissue or nerve injury is a common clinical symptom. Although intensive research on the neurobiological mechanisms of chronic pain has been carried out during previous decades, this disorder is still poorly managed by current drugs such as opioids and non-steroidal anti-inflammatory drugs. Inflammation-, tissue injury-, and/or nerve injury-induced changes in gene expression in sensory neurons of the dorsal root ganglion (DRG), spinal cord dorsal horn, and pain-associated brain regions are thought to participate in chronic pain genesis; however, how these changes occur is still elusive. Epigenetic modifications including DNA methylation and covalent histone modifications control gene expression. Recent studies have shown that peripheral noxious stimulation changes DNA methylation and histone modifications and that these changes may be related to the induction of pain hypersensitivity under chronic pain conditions. This review summarizes the current knowledge and progress in epigenetic research in chronic pain and discusses the potential role of epigenetic modifications as therapeutic antinociceptive targets in this disorder.

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“…Many factors—most not well understood—can alter histone–gene interactions and gene regulation. Chromatin and histones control gene expression in all reproductive and somatic cells, but their actions in neurons and neuronal support structures are most critical for understanding gene regulation in central nervous system (CNS) development, behavior, stress adaptation, and motivation …”

Section: Crh Stress and Addictionmentioning

confidence: 99%

Addiction and corticotropin‐releasing hormone type 1 receptor antagonist medications

Contoreggi

Lee

Chrousos

2013

Annals of the New York Academy of Sciences

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Derangements in corticotropin-releasing hormone (CRH) through its type 1 receptor (CRHR1) have been identified in many pathologic conditions. Preclinical models of addiction find that small-molecule antagonists of CRHR1 can limit induction, maintenance, and relapse to drugs of abuse. Neuropsychiatric clinical trials of CRHR1 antagonists have shown mixed efficacy; treatment of addictive disorders has not been established, but finding effective treatments for addictive disorders is critical. Establishing effectiveness for substance abuse treatment will require a different design approach than was used for depression and anxiety trials. Focusing on active versus passive outcome measures, such as resilience to external stressful stimuli, may provide signals in curbing craving and relapse. Study design should include measures of abstinence and drug exposure, but additional elements of stress prevention should also be incorporated. Agents that could provide preemptive protection from drug use and relapse are novel and untested. An understanding of the evolutionary significance of the stress system and preclinical models suggests that these agents may provide protection in this manner. Investigators designing future trials might refocus their understanding of addiction and treatment in this new direction.

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Methylation, memory and addiction

Cited by 28 publications

References 38 publications

The landscape of DNA methylation amid a perfect storm of autism aetiologies

The landscape of DNA methylation amid a perfect storm of autism aetiologies

Epigenetic Regulation of Chronic Pain

Addiction and corticotropin‐releasing hormone type 1 receptor antagonist medications

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