Methamphetamine Induces Dynamic Changes of Histone Deacetylases in Different Phases of Behavioral Sensitization

Li, Hui; Li, Fēi; Wu, Ning; Su, Rui‐Bin; Li, Jin

doi:10.1111/cns.12301

Cited by 11 publications

(18 citation statements)

References 10 publications

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“…Chronic METH also reduced the expression of the class II HDAC, HDAC4, without any effect on HDAC5. 66 Both HDAC4 and HDAC5 expression was decreased when measured at 7 days of withdrawal from METH treatment. Chronic METH also increased expression of two class III HDACs, SIRT1 and SIRT2, in the dorsal striatum.…”

Section: Self-administration (3-4 Weeks; 4-h Session)mentioning

confidence: 96%

“…31 The role of HDAC1 and HDAC2 in the acute effects of amphetamine-like drugs is also supported by a behavioral study that an HDAC1/2 inhibitor, Cp60, was able to inhibit amphetamine (AMPH)-induced locomotion. 65 In a recent report, Li et al 66 also provided evidence that a single METH injection decreased HDAC1 and HDAC2 in the prefrontal cortex. The epigenetic effects of repeated METH exposure have also been investigated in a model of increasing METH doses over weeks 4 (see Figure 1).…”

Section: Self-administration (3-4 Weeks; 4-h Session)mentioning

confidence: 97%

“…Of note is that valproic acid, a histone deacetylase inhibitor, which is used in the treatment of various neuropsychiatric disorders, was able to block METH‐induced decreased expression of AMPA receptor subunits. In contrast, chronic METH decreased HDAC2 expression in the prefrontal cortex, suggesting that neuroscientists and pharmacologists need to be cognizant of the brain regions being investigated when studying models of addiction or drug effects because of the diversity of responses that drugs can cause. Chronic METH also reduced the expression of the class II HDAC, HDAC4, without any effect on HDAC5 .…”

Section: Role Of Epigenetics In Psychostimulant Exposurementioning

confidence: 99%

“…In contrast, chronic METH decreased HDAC2 expression in the prefrontal cortex, suggesting that neuroscientists and pharmacologists need to be cognizant of the brain regions being investigated when studying models of addiction or drug effects because of the diversity of responses that drugs can cause. Chronic METH also reduced the expression of the class II HDAC, HDAC4, without any effect on HDAC5 . Both HDAC4 and HDAC5 expression was decreased when measured at 7 days of withdrawal from METH treatment.…”

Section: Role Of Epigenetics In Psychostimulant Exposurementioning

confidence: 99%

“…68 ChIP / polymerase chain reaction (PCR) also showed that METH decreased the enrichment of acetylated histone H4 on AMPA receptors and of histone deacetylase 2 enrichment onto GluA1 and GluA2 gene sequences. Of note is that valproic acid, a histone deacetylase inhibitor, which is used in the treatment of various neuropsychiatric disorders, 69 prefrontal cortex, 66 suggesting that neuroscientists and pharmacologists need to be cognizant of the brain regions being investigated when studying models of addiction or drug effects because of the diversity of responses that drugs can cause. Chronic METH also reduced the expression of the class II HDAC, HDAC4, without any effect on HDAC5.…”

Section: Self-administration (3-4 Weeks; 4-h Session)mentioning

confidence: 99%

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Epigenetics and addiction

Cadet

McCoy

Jayanthi

2016

Clin Pharma and Therapeutics

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Addictions are public health menaces. However, despite advances in addiction research, the cellular or molecular mechanisms that cause transition from recreational use to addiction remain to be elucidated. We have recently suggested that addiction may be secondary to long-term epigenetic modifications that determine the clinical course of substance use disorders. A better understanding of epigenetic mechanisms in animal models that mimic human conditions should help to usher in a new area of drug development against addiction.

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Section: Self-administration (3-4 Weeks; 4-h Session)mentioning

confidence: 96%

Section: Self-administration (3-4 Weeks; 4-h Session)mentioning

confidence: 97%

Section: Role Of Epigenetics In Psychostimulant Exposurementioning

confidence: 99%

Section: Role Of Epigenetics In Psychostimulant Exposurementioning

confidence: 99%

Section: Self-administration (3-4 Weeks; 4-h Session)mentioning

confidence: 99%

See 3 more Smart Citations

Epigenetics and addiction

Cadet

McCoy

Jayanthi

2016

Clin Pharma and Therapeutics

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The Class II Histone Deacetylase Hypothesis of Addiction

Griffin

Melas

Kandel

et al. 2018

Biological Psychiatry

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Repeated methamphetamine and modafinil induce differential cognitive effects and specific histone acetylation and DNA methylation profiles in the mouse medial prefrontal cortex

González

Jayanthi²,

Gómez

et al. 2018

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Methamphetamine (METH) and modafinil are psychostimulants with different long-term cognitive profiles: METH is addictive and leads to cognitive decline, whereas modafinil has little abuse liability and is a cognitive enhancer. Increasing evidence implicates epigenetic mechanisms of gene regulation behind the lasting changes that drugs of abuse and other psychotropic compounds induce in the brain, like the control of gene expression by histones 3 and 4 tails acetylation (H3ac and H4ac) and DNA cytosine methylation (5-mC). Mice were treated with a seven-day repeated METH, modafinil or vehicle protocol and evaluated in the novel object recognition (NOR) test or sacrificed 4days after last injection for molecular assays. We evaluated total H3ac, H4ac and 5-mC levels in the medial prefrontal cortex (mPFC), H3ac and H4ac promotor enrichment (ChIP) and mRNA expression (RT-PCR) of neurotransmitter systems involved in arousal, wakefulness and cognitive control, like dopaminergic (Drd1 and Drd2), α-adrenergic (Adra1a and Adra1b), orexinergic (Hcrtr1 and Hcrtr2), histaminergic (Hrh1 and Hrh3) and glutamatergic (AMPA Gria1 and NMDA Grin1) receptors. Repeated METH and modafinil treatment elicited different cognitive outcomes in the NOR test, where modafinil-treated mice performed as controls and METH-treated mice showed impaired recognition memory. METH-treated mice also showed i) decreased levels of total H3ac and H4ac, and increased levels of 5-mC, ii) decreased H3ac enrichment at promoters of Drd2, Hcrtr1/2, Hrh1 and Grin1, and increased H4ac enrichment at Drd1, Hrh1 and Grin1, iii) increased mRNA of Drd1a, Grin1 and Gria1. Modafinil-treated mice shared none of these effects and showed increased H3ac enrichment and mRNA expression at Adra1b. Modafinil and METH showed similar effects linked to decreased H3ac in Hrh3, increased H4ac in Hcrtr1, and decreased mRNA expression of Hcrtr2. The specific METH-induced epigenetic and transcriptional changes described here may be related to the long-term cognitive decline effects of the drug and its detrimental effects on mPFC function. The lack of similar epigenetic effects of chronic modafinil administration supports this notion.

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Methamphetamine Induces Dynamic Changes of Histone Deacetylases in Different Phases of Behavioral Sensitization

Cited by 11 publications

References 10 publications

Epigenetics and addiction

Epigenetics and addiction

The Class II Histone Deacetylase Hypothesis of Addiction

Repeated methamphetamine and modafinil induce differential cognitive effects and specific histone acetylation and DNA methylation profiles in the mouse medial prefrontal cortex

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