Histone Deacetylases (HDAC)‐Induced Histone Modifications in the Amygdala: A Role in Rapid Tolerance to the Anxiolytic Effects of Ethanol

Sakharkar, Amul J.; Zhang, Huaibo; Tang, Lei; Shi, Guang; Pandey, Subhash C.

doi:10.1111/j.1530-0277.2011.01581.x

Cited by 114 publications

(188 citation statements)

References 56 publications

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“…Moreover, chronic exposure to ethanol leads to inhibition of HDAC activity in the amygdala and to a rapid tolerance to the anxiolytic effects of ethanol (108,109). Furthermore, treatment of rats with a potent HDAC inhibitor (trichostatin A) decreases anxiety-like symptoms observed during ethanol withdrawal after chronic exposure (108). Taken together, these results support the fact that histone acetylation plays a crucial role in the rapid tolerance to the anxiolytic effects of ethanol that may promote drinking.…”

Section: Drugssupporting

confidence: 73%

“…Ethanol increases global levels of H3 and H4 acetylation in the prefrontal cortex, nucleus accumbens, and amygdala of ethanol-exposed rats (107,108). Moreover, chronic exposure to ethanol leads to inhibition of HDAC activity in the amygdala and to a rapid tolerance to the anxiolytic effects of ethanol (108,109). Furthermore, treatment of rats with a potent HDAC inhibitor (trichostatin A) decreases anxiety-like symptoms observed during ethanol withdrawal after chronic exposure (108).…”

Section: Drugsmentioning

confidence: 99%

“…Indeed, there is a clear association between chronic ethanol exposure and altered histone acetylation (106). Ethanol increases global levels of H3 and H4 acetylation in the prefrontal cortex, nucleus accumbens, and amygdala of ethanol-exposed rats (107,108). Moreover, chronic exposure to ethanol leads to inhibition of HDAC activity in the amygdala and to a rapid tolerance to the anxiolytic effects of ethanol (108,109).…”

Section: Drugsmentioning

confidence: 99%

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Histone acetylation in neuronal (dys)function

Bonnaud¹,

Suberbielle²,

Malnou³

2016

Biomolecular Concepts

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Abstract:Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene expression. Epigenetic modifications have been shown to play an important role in numerous neuronal functions, from synaptic plasticity to learning and memory. In particular, histone acetylation is a central player in these processes. In this review, we present the molecular mechanisms of histone acetylation and summarize the data underlying the relevance of histone acetylation in cognitive functions in normal and pathological conditions. In the last part, we discuss the different mechanisms underlying the dysregulation of histone acetylation associated with neurological disorders, with a particular focus on environmental causes (stress, drugs, or infectious agents) that are linked to impaired histone acetylation.

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Section: Drugssupporting

confidence: 73%

Section: Drugsmentioning

confidence: 99%

Section: Drugsmentioning

confidence: 99%

See 1 more Smart Citation

Histone acetylation in neuronal (dys)function

Bonnaud¹,

Suberbielle²,

Malnou³

2016

Biomolecular Concepts

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“…Modification of gene expression is associated with the progression to addiction (9,10). Epigenetic changes have been implicated in alcohol-dependent gene regulation (11), in the development of rapid tolerance to ethanol in a variety of model systems (12)(13)(14), and in alcohol-drinking behaviors in mammals (11,15). Epigenetic factors also may modify the basal LR to alcohol.…”

mentioning

confidence: 99%

SWI/SNF chromatin remodeling regulates alcohol response behaviors in Caenorhabditis elegans and is associated with alcohol dependence in humans

Mathies¹,

Blackwell²,

Austin³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Alcohol abuse is a widespread and serious problem. Understanding the factors that influence the likelihood of abuse is important for the development of effective therapies. There are both genetic and environmental influences on the development of abuse, but it has been difficult to identify specific liability factors, in part because of both the complex genetic architecture of liability and the influences of environmental stimuli on the expression of that genetic liability. Epigenetic modification of gene expression can underlie both genetic and environmentally sensitive variation in expression, and epigenetic regulation has been implicated in the progression to addiction. Here, we identify a role for the switching defective/sucrose nonfermenting (SWI/SNF) chromatin-remodeling complex in regulating the behavioral response to alcohol in the nematode Caenorhabditis elegans. We found that SWI/SNF components are required in adults for the normal behavioral response to ethanol and that different SWI/SNF complexes regulate different aspects of the acute response to ethanol. We showed that the SWI/SNF subunits SWSN-9 and SWSN-7 are required in neurons and muscle for the development of acute functional tolerance to ethanol. Examination of the members of the SWI/SNF complex for association with a diagnosis of alcohol dependence in a human population identified allelic variation in a member of the SWI/SNF complex, suggesting that variation in the regulation of SWI/SNF targets may influence the propensity to develop abuse disorders. Together, these data strongly implicate the chromatin remodeling associated with SWI/SNF complex members in the behavioral responses to alcohol across phyla.SWI/SNF | alcohol | C. elegans | chromatin remodeling | GWAS

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“…NPY is anxiolytic and may mediate acute ethanol-induced anxiolysis. By using histone deacetylase inhibitors, Sakharkar et al (2012) showed in alcohol-preferring P rats that a rapid tolerance is produced to this anxiolytic effect during chronic ethanol treatment via possible epigenetic changes causing a reduction in NPY expression. It is quite possible that these epigenetic changes are far more frequent and affect the transcription of many genes important for plasticity (Nestler, 2014) and that epigenetic mechanisms can also contribute to genetic vulnerability to increased alcohol consumption, at least in animal models (Moonat et al, 2013).…”

Section: Ethanol Administered In Vitro Enhanced Ipsps Andmentioning

confidence: 99%