J 2009

Dynamic DNA methylation programs persistent adverse effects of early-life stress

MURGATROYD, Chris; Alexandre V PATCHEV; Yonghe WU; Vincenzo MICALE; Yvonne BOCKMUHL et al.

Základní údaje

Originální název

Dynamic DNA methylation programs persistent adverse effects of early-life stress

Autoři

MURGATROYD, Chris; Alexandre V PATCHEV; Yonghe WU; Vincenzo MICALE; Yvonne BOCKMUHL; Dieter FISCHER; Florian HOLSBOER; Carsten T WOTJAK; Osborne F X ALMEIDA a Dietmar SPENGLER

Vydání

Nature Neuroscience, NEW YORK, NATURE PUBLISHING GROUP, 2009, 1097-6256

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30000 3. Medical and Health Sciences

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 14.345

Označené pro přenos do RIV

Ne

Klíčová slova anglicky

PITUITARY-ADRENAL AXIS; GENE-EXPRESSION; MOUSE MODEL; EPIGENETIC REGULATION; BDNF TRANSCRIPTION; RETT-SYNDROME; DISORDERS; ANXIETY; MECP2; BRAIN

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 7. 8. 2012 08:20, Olga Křížová

Anotace

V originále

Adverse early life events can induce long-lasting changes in physiology and behavior. We found that early-life stress (ELS) in mice caused enduring hypersecretion of corticosterone and alterations in passive stress coping and memory. This phenotype was accompanied by a persistent increase in arginine vasopressin (AVP) expression in neurons of the hypothalamic paraventricular nucleus and was reversed by an AVP receptor antagonist. Altered Avp expression was associated with sustained DNA hypomethylation of an important regulatory region that resisted age-related drifts in methylation and centered on those CpG residues that serve as DNA-binding sites for the methyl CpG-binding protein 2 (MeCP2). We found that neuronal activity controlled the ability of MeCP2 to regulate activity-dependent transcription of the Avp gene and induced epigenetic marking. Thus, ELS can dynamically control DNA methylation in postmitotic neurons to generate stable changes in Avp expression that trigger neuroendocrine and behavioral alterations that are frequent features in depression.