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pubmed, article, google, scholar, histone, stress, cas, depression, chronic, acetylation, methylation, social, hdac, central, epigenetic, defeat, nac, expression, hippocampus, studies, decreased, study, gene, models, levels, antidepressant, treatment, bdnf, chromatin, increased, brain, role, genes, regions, animals, covington, neurosci, hkme, regulation, molecular, patients, depressed, nestler, mice, effects, observed, modifications, psychiatry, global, nature,

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n-methyl-d-aspartate/extracellular signal-regulated kinase/mitogen nature portfolio permissions reprints privacy policy basic research advertising research subjective nature social media nature 387 nature 447 nature 455 nature 403 nature regional specificity wnt-dishevelled-gsk3beta signaling cascade genome-wide association data brain-derived neurotrophic factor author correspondence anna-monika-prize paper perceptual attentional set-shifting unpublished genome-wide data corticotropin-releasing factor gene cortical-striatal-limbic circuit cortical-striatal-limbic circuitry study utilized chip-chip lacks s-nitrosylation sites atp-dependent chromatin remodelers american psychiatric association atp-dependent remodeling enzymes long-lasting behavioral consequences long-lasting behavioural forced swimming test central inflammatory cytokines low crh/ne states permissions ras-mapk-creb signaling g9a exerted pro-depressant epigenetic language stress-related memory formation major depressive disorder complex language n-terminal histone tails histone n-termini tails prolonged social isolation widespread h3k9/k27 methylation receptor tyrosine kinase behavioural-neurobiological concordance atp-dependent remodelers stress-regulated transcription factors

Questions {❓}

• Histone acetylation: truth of consequences?
• INTRODUCTION: WHY EPIGENETICS?
• The above sections reviewed global changes in histone acetylation and methylation machineries in various depression models, but the far more important functional question is: at what specific genes or intergenic regions does such regulation occur to control depression-related behavior?

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         description:Major depressive disorder is a chronic, remitting syndrome involving widely distributed circuits in the brain. Stable alterations in gene expression that contribute to structural and functional changes in multiple brain regions are implicated in the heterogeneity and pathogenesis of the illness. Epigenetic events that alter chromatin structure to regulate programs of gene expression have been associated with depression-related behavior, antidepressant action, and resistance to depression or ‘resilience’ in animal models, with increasing evidence for similar mechanisms occurring in postmortem brains of depressed humans. In this review, we discuss recent advances in our understanding of epigenetic contributions to depression, in particular the role of histone acetylation and methylation, which are revealing novel mechanistic insight into the syndrome that may aid in the development of novel targets for depression treatment.
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