Effect of the histone deacetylase inhibitors on behavioural sensitization to a single morphine exposure in mice

Li, Jing; Luo, Juan; Zhang, Min; Qin, Wangjun; Li, Yuling; Liu, Qing; Wang, Yanting; Lawrence, Andrew J; Liang, Jing

doi:10.1016/j.neulet.2011.03.005

Cited by 39 publications

(24 citation statements)

References 30 publications

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“…The present findings are in line with previous studies showing that histone deacetylase inhibition results in the reversal of a number of measures of behavioral plasticity linked with opioid addiction, viz. behavioral sensitization associated with single morphine exposure (Jing et al 2011), morphine-induced locomotor sensitization and conditioned place preference (SanchisSegura et al 2009;Wang et al 2010). Therefore, the present data in corroboration with the previous studies implicate that histone-deacetylase-mediated deacetylation of histone protein, possibly H3, might be associated with the pathogenesis of the development of opioid withdrawal syndrome in opioid-dependent subjects.…”

Section: Discussionsupporting

confidence: 91%

Modulation of histone deacetylase attenuates naloxone-precipitated opioid withdrawal syndrome

Rehni

Singh

Rachamalla

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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The present study has been designed to investigate the effect of selective inhibitors of histone deacetylase and/or N-acetyl-Asp-Glu-Val-Asp-al (Ac-DEVD-CHO), a selective interleukin-1β converting enzyme inhibitor, on the development of naloxone-induced opioid withdrawal syndrome both in vitro and in vivo and the effect of histone deacetylase inhibition on histone H3 acetylation in brain. Sub-acute morphine administration followed by a single injection of naloxone (8 mg/kg, i.p.) was used to precipitate opioid withdrawal syndrome in mice. Behavioral observations were made immediately after naloxone treatment. Withdrawal syndrome was quantitatively assessed in terms of withdrawal severity score and frequency of jumping, rearing, fore paw licking and circling. Separately naloxone-induced contraction in morphine-dependent isolated rat ileum was employed as an in vitro model. An isobolographic study design was employed to assess potential synergistic activity between trichostatin A and Ac-DEVD-CHO. Brain histone acetylation status was examined by western blotting. Injection of naloxone precipitated a severe form of abstinence syndrome in morphine-dependent mice along with strong contracture in isolated rat ileum. Administration of tributyrin (1.5, 3 and 6 g/kg, p.o.), trichostatin A (0.3, 1.0 and 3.0 mg/kg, p.o.) and Ac-DEVD-CHO (0.3, 1.0 and 3.0 mg/kg, p.o.) markedly and dose dependently attenuated naloxone-induced morphine withdrawal syndrome in vivo as well as in vitro in rat ileum. Trichostatin A was also observed to exert a synergistic interaction with Ac-DEVD-CHO. Western blot analysis revealed that multiple administration with the effective dose of tributyrin or trichostatin A in the in vivo experiments induced hyperacetylation of histone H3 in the mouse brain. Thus, it is proposed that histone deacetylase activation linked mechanism might be involved in the development of opioid dependence and the precipitation of its withdrawal syndrome.

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Section: Discussionsupporting

confidence: 91%

Modulation of histone deacetylase attenuates naloxone-precipitated opioid withdrawal syndrome

Rehni

Singh

Rachamalla

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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“…In closer relation to our work, early repeated maternal deprivation increases opiate consumption in adult rats through epigenetic modifications that enhance HDAC expression and activity in the NAc and treatment with the HDACi sodium valproate normalized opioid consumption (Tesone-Coelho et al 2015). HDACis have also been shown to facilitate extinction of conditioned place preference and reduce development of morphine behavioral sensitization in rodents exposed to morphine (Jing et al 2011;Wang et al 2010). Furthermore, specific knockdown of class I HDACs suppresses cocaineinduced behavioral plasticity through a chromatin-mediated decrease in GABAergic inhibition in the NAc (Kennedy et al 2013).…”

Section: Discussionsupporting

confidence: 73%

“…Acute and chronic administration of psychostimulants and morphine elicits histone modifications such as histone acetylation at a specific subset of learningassociated genes in the brain reward circuitry including the VTA that could facilitate and consolidate lasting neural and behavioral plasticity induced by drug abuse. Moreover, increasing histone acetylation through pre-or coadministration of histone deacetylase (HDAC) inhibitors (HDACis) in conjunction with abused drugs promotes or opposes drug-induced synaptic and behavioral abnormalities, suggesting that this epigenetic mark might be required to potentiate or prevent an addicted state (Jing et al 2011;Kalda et al 2007; Kennedy et al 2013;Kumar et al 2005;Levine et al 2005;Renthal et al 2007Renthal et al , 2009Sanchis-Segura et al 2009;Sun et al 2012;Wang et al 2010). This opens the possibility of targeting epigenetic mechanisms during initial learning or memory retrieval of drug-associated cues as a novel pharmacological therapy for extinction of drug-seeking behaviors.…”

Section: Learning Mechanisms In Brain Reward Pathways Are Hijacked Afmentioning

confidence: 99%

Morphine-induced synaptic plasticity in the VTA is reversed by HDAC inhibition

Authement

Langlois

Kassis

et al. 2016

Journal of Neurophysiology

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Dopamine (DA) dysfunction originating from the ventral tegmental area (VTA) occurs as a result of synaptic abnormalities following consumption of drugs of abuse and underlies behavioral plasticity associated with drug abuse. Drugs of abuse can cause changes in gene expression through epigenetic mechanisms in the brain that underlie some of the lasting neuroplasticity and behavior associated with addiction. Here we investigated the function of histone acetylation and histone deacetylase (HDAC)2 in the VTA in recovery of morphine-induced synaptic modifications following a single in vivo exposure to morphine. Using a combination of immunohistochemistry, Western blot, and whole cell patch-clamp recording in rat midbrain slices, we show that morphine increased HDAC2 activity in VTA DA neurons and reduced histone H3 acetylation at lysine 9 (Ac-H3K9) in the VTA 24 h after the injection. Morphine-induced synaptic changes at glutamatergic synapses involved endocannabinoid signaling to reduce GABAergic synaptic strength onto VTA DA neurons. Both plasticities were recovered by in vitro incubation of midbrain slices with a class I-specific HDAC inhibitor (HDACi), CI-994, through an increase in acetylation of histone H3K9. Interestingly, HDACi incubation also increased levels of Ac-H3K9 and triggered GABAergic and glutamatergic plasticities in DA neurons of saline-treated rats. Our results suggest that acute morphine-induced changes in VTA DA activity and synaptic transmission engage HDAC2 activity locally in the VTA to maintain synaptic modifications through histone hypoacetylation. ventral tegmental area; synaptic plasticity; electrophysiology; synaptic transmission; histone deacetylase

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“…Quite interestingly, HDAC inhibitors also modulate behavioral outcomes of opioid drugs such as acute morphine-induced hyperactivity, opioid dependence, the development of behavioral sensitization, and the precipitation of morphine withdrawal syndrome in vivo (Sanchis-Segura et al, 2009;Jing et al, 2011;Rehni et al, 2012). In addition, emerging studies suggest that HDAC inhibitors facilitate the extinction of rewarding memory of drug taking (Wang et al, 2012), and drug-induced conditioned place preference .…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Activation of μ-Opioid Receptor Gene via Increased Expression and Function of Mitogen- and Stress-Activated Protein Kinase 1

Wagley

Law

et al. 2017

Mol Pharmacol

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Since the discovery of m-opioid receptor (MOR) gene two decades ago, various regulatory factors have been shown to interact with the MOR promoter and modulate transcript levels. However, the majority of early transcriptional studies on MOR gene have not addressed how intracellular signaling pathways mediate extracellular modulators. In this study, we demonstrate that MOR epigenetic regulation requires multiple coordinated signals converging at the MOR promoter, involving mitogenactivated protein kinase (MAPK) activation and mitogen-and stress-activated protein kinase 1 (MSK1)-ranges of intracellular signaling pathways similar to those activated by opioid agonists. Inhibiting p38 MAPK or extracellular signal-regulated kinase (ERK) 1/2 MAPK (upstream activators of MSK1) reduced MOR expression levels; accordingly, the functional role of MSK1, but not MSK2, was demonstrated using genetic approaches. However, for maximal MSK1 effect, an open chromatin configuration was required, because in vitro CpG methylation of the MOR promoter abolished MSK1 activity. Finally, endogenous MSK1 levels concomitantly increased to regulate MOR gene expression during neuronal differentiation of P19 cells, suggesting a conserved role of this kinase in the epigenic activation of MOR in neurons. Taken together, our findings indicate that the expression of MOR gene requires the activity of intracellular signaling pathways that have been implicated in the behavioral outcomes of opioid drugs, which suggests that an autoregulatory mechanism may function in opioid systems.

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Effect of the histone deacetylase inhibitors on behavioural sensitization to a single morphine exposure in mice

Cited by 39 publications

References 30 publications

Modulation of histone deacetylase attenuates naloxone-precipitated opioid withdrawal syndrome

Modulation of histone deacetylase attenuates naloxone-precipitated opioid withdrawal syndrome

Morphine-induced synaptic plasticity in the VTA is reversed by HDAC inhibition

Epigenetic Activation of μ-Opioid Receptor Gene via Increased Expression and Function of Mitogen- and Stress-Activated Protein Kinase 1

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