Morphine withdrawal produces ERK-dependent and ERK-independent epigenetic marks in neurons of the nucleus accumbens and lateral septum

Ciccarelli, Alessandro; Calza, Arianna; Santoru, F; Grasso, Fabrizio; Concas, Alessandra; Sassoè‐Pognetto, Marco; Giustetto, Maurizio

doi:10.1016/j.neuropharm.2012.12.010

Cited by 37 publications

(29 citation statements)

References 78 publications

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“…ERK1/2 is known to alter several epigenetic markers and transcription factors including c-fos , brain-derived neurotrophic factor, and cAMP response element binding proteins (CREB) in several brain regions following opioid withdrawal (Wang et al, 2012, Ciccarelli et al, 2013). The adenylyl cyclase-cAMP-CREB pathway is upregulated following prolonged opioid exposure (Cao et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Ligand-biased activation of extracellular signal-regulated kinase 1/2 leads to differences in opioid induced antinociception and tolerance

Bobeck

Ingram

Hermes

et al. 2016

Behavioural Brain Research

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Opioids produce antinociception by activation of G protein signaling linked to the mu-opioid receptor (MOPr). However, opioid binding to the MOPr also activates β-arrestin signaling. Opioids such as DAMGO and fentanyl differ in their relative efficacy for activation of these signaling cascades, but the behavioral consequences of this differential signaling are not known. The purpose of this study was to evaluate the behavioral significance of G protein and internalization dependent signaling within ventrolateral periaqueductal gray (vlPAG). Antinociception induced by microinjecting DAMGO into the vlPAG was attenuated by blocking Gαi/o protein signaling with administration of pertussis toxin (PTX), preventing internalization with administration of dynamin dominant-negative inhibitory peptide (dyn-DN) or direct inhibition of ERK1/2 with administration of the MEK inhibitor, U0126. In contrast, the antinociceptive effect of microinjecting fentanyl into the vlPAG was not altered by administration of PTX or U0126, and was enhanced by administration of dyn-DN. Microinjection of DAMGO, but not fentanyl, into the vlPAG induced phosphorylation of ERK1/2, which was blocked by inhibiting receptor internalization with administration of dyn-DN, but not by inhibition of Gαi/o proteins. ERK1/2 inhibition also prevented the development and expression of tolerance to repeated DAMGO microinjections, but had no effect on fentanyl tolerance. These data reveal that ERK1/2 activation following MOPr internalization contributes to the antinociceptive effect of some (e.g., DAMGO), but not all opioids (e.g., fentanyl) despite the known similarities for these agonists to induce β-arrestin recruitment and internalization.

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Section: Discussionmentioning

confidence: 99%

Ligand-biased activation of extracellular signal-regulated kinase 1/2 leads to differences in opioid induced antinociception and tolerance

Bobeck

Ingram

Hermes

et al. 2016

Behavioural Brain Research

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“…Within 1 hour after the last administration of morphine, morphine was in vivo precipitated by naloxone. Such precipitation results in different dynamics of H3 phosphorylation and acetylation: H3 phosphorylation was increased significantly while H3 acetylation remained unchanged [84].…”

Section: A Specific Examples Of Exposures and Effects On Histone Modmentioning

confidence: 99%

Histone Modification Patterns and Their Responses to Environment

Dai

Wang

2014

Curr Envir Health Rpt

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Histone modifications play important roles in the epigenetic regulation of gene expression. Recent genomewide profiling of histone modifications with deep sequencingbased methods provides novel insights of crosstalk between histone modifications, leading to recent proposals of histone "language" or "web" as an alternative of "code" to appreciate combinatorial modification patterns. Environmental factor-altered histone modifications now may be addressed dynamically and systematically with the recognition and use of these interesting combinatorial patterns.

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“…Despite these effects, no evidence exists to show that opiate consumption causes DNA alteration; however, recent studies have shown that chronic exposure to opiates affects chromatin-related proteins and therefore induces modifications in gene expression patterns. In fact, chronic morphine exposure causes epigenetic modifications (12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

Amri

Sadegh

Moulaei

et al. 2017

The American Journal of Drug and Alcohol Abuse

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Morphine withdrawal produces ERK-dependent and ERK-independent epigenetic marks in neurons of the nucleus accumbens and lateral septum

Cited by 37 publications

References 78 publications

Ligand-biased activation of extracellular signal-regulated kinase 1/2 leads to differences in opioid induced antinociception and tolerance

Ligand-biased activation of extracellular signal-regulated kinase 1/2 leads to differences in opioid induced antinociception and tolerance

Histone Modification Patterns and Their Responses to Environment

Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

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