Behavioral sensitization induced by methamphetamine causes differential alterations in gene expression and histone acetylation of the prefrontal cortex in rats

Li, Hui; Chen, Jing-An; Ding, Qiao; Lu, Guan-Yi; Wu, Ning; Su, Rui‐Bin; Li, Fēi; Li, Jin

doi:10.1186/s12868-021-00616-5

Cited by 15 publications

(12 citation statements)

References 55 publications

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“…These results support the notion that enrichment at gene promoters is not directly related to the levels of the histone protein under investigation. A recent ChIP-chip analysis using a rat model of METH-induced behavioral sensitization discovered increased H3 acetylation in a large number of gene promoters (241 genes) and increased H4 acetylation in a fewer number of gene promoters (10 genes) in the pCTX [65]. Interestingly, H4 hyperacetylation was found to contribute to increased expression of Angp32a, a gene is involved in the regulation of synaptic plasticity and memory [65].…”

Section: Chronic Effects Of Meth On Histone Acetylationmentioning

confidence: 99%

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Epigenetic Regulatory Dynamics in Models of Methamphetamine-Use Disorder

Jayanthi

McCoy

Cadet

2021

Genes

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Methamphetamine (METH)-use disorder (MUD) is a very serious, potentially lethal, biopsychosocial disease. Exposure to METH causes long-term changes to brain regions involved in reward processing and motivation, leading vulnerable individuals to engage in pathological drug-seeking and drug-taking behavior that can remain a lifelong struggle. It is crucial to elucidate underlying mechanisms by which exposure to METH leads to molecular neuroadaptive changes at transcriptional and translational levels. Changes in gene expression are controlled by post-translational modifications via chromatin remodeling. This review article focuses on the brain-region specific combinatorial or distinct epigenetic modifications that lead to METH-induced changes in gene expression.

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Section: Chronic Effects Of Meth On Histone Acetylationmentioning

confidence: 99%

“…METH use is known to be accompanied with behavioral sensitization that can last for several weeks to months in rodents [65,70]. Interestingly, the class I HDACi, valproic acid (VPA), can attenuate behavioral sensitization responses [71].…”

Section: Role Of Hdac Inhibitors In Meth Exposurementioning

confidence: 99%

Epigenetic Regulatory Dynamics in Models of Methamphetamine-Use Disorder

Jayanthi

McCoy

Cadet

2021

Genes

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“…Consistent with previous studies, we found that METH F1 , which is insufficient to induce CPP in naïve mice, effectively induced METH-preferred behaviors in METH-sired male F1 and not in SAL-sired male F1, indicating an enhanced sensitivities to drugs in F1 of sires exposed to METH. The mPFC has been implicated in the vulnerability to drug abuse [6][7][8]. Currently, little literature uncover the association of paternal METH intake with offspring mPFC alteration.…”

Section: Discussionmentioning

confidence: 99%

“…The medial prefrontal cortex (mPFC) is critically implicated in the processes of METH addiction [4, 5] and susceptibility to drugs [6–8]. Human imaging studies show that prenatal METH exposure significantly affect the volume, cortical thickness and connection of offspring brains, especially the prefrontal cortex (PFC) [7, 9, 10]. Previously, we found that mPFC were blunted to stimulants in METH-sired mice during adulthood [11].…”

Section: Introductionmentioning

confidence: 99%

Paternal methamphetamine exposure induces higher sensitivity to methamphetamine in male offspring through driving ADRB1 on CaMKII-positive neurons in mPFC

Zheng

Wen

et al. 2022

Preprint

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As a highly addictive psychostimulant drug, paternal methamphetamine (METH) exposure enhances the risk of developing addiction to drugs in descendants, however the underlying mechanism remains unclear. Medial prefrontal cortex (mPFC) is a key brain region that implicated in susceptibility to drugs. Here, male adult mice were exposed to METH for 30 days, followed by mating with naive female mice to create the first-generation (F1) mice. In METH-sired mice, baseline levels of c-Fos were decreased but β1-adrenergic receptor (ADRB1) were increased in mPFC by paternal METH exposure. Trained with subthreshold-dosed administration of METH, METH-sired mice exhibited significant METH-preferred behaviors, accompanied with higher levels of c-Fos, ADRB1 and dendritic spines density in mPFC. Importantly, local blocking ADRB1 activity or specific knockdown of ADRB1 on excitatory neurons of mPFC, both efficiently inhibited METH-preferred behaviors in METH-sired mice. In parallel, levels of p-ERK1/2 and ΔFosB, as well as dendritic spine density were reduced by knocking-down mPFC ADRB1 in METH-sired mice. Collectively, these findings suggested that targeting ADRB1 signals in mPFC may represent a promising therapeutic strategy for preventing drug addiction, particularly in progeny with a history of paternal drugs exposure.

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“…Methamphetamine (MA) is synthesized on the basis of ephedrine, which has the effect of mental stimulation ( Chen et al, 2021 ). MA is one of the most widely abused illegal substances in the world, but unfortunately, there are still very few studies on detoxification after a period of time ( Huang et al, 2021 ; Li et al, 2021 ). Due to the high addiction, it is prohibited in many countries.…”

Section: Introductionmentioning

confidence: 99%

Identification of Methamphetamine Abstainers by Resting-State Functional Magnetic Resonance Imaging

Dong

Huang

et al. 2021

Front. Psychol.

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Methamphetamine (MA) can cause brain structural and functional impairment, but there are few studies on whether this difference will sustain on MA abstainers. The purpose of this study is to investigate the correlation of brain networks in MA abstainers. In this study, 47 people detoxified for at least 14 months and 44 normal people took a resting-state functional magnetic resonance imaging (RS-fMRI) scan. A dynamic (i.e., time-varying) functional connectivity (FC) is obtained by applying sliding windows in the time courses on the independent components (ICs). The windowed correlation data for each IC were then clustered by k-means. The number of subjects in each cluster was used as a new feature for individual identification. The results show that the classifier achieved satisfactory performance (82.3% accuracy, 77.7% specificity, and 85.7% sensitivity). We find that there are significant differences in the brain networks of MA abstainers and normal people in the time domain, but the spatial differences are not obvious. Most of the altered functional connections (time-varying) are identified to be located at dorsal default mode network. These results have shown that changes in the correlation of the time domain may play an important role in identifying MA abstainers. Therefore, our findings provide valuable insights in the identification of MA and elucidate the pathological mechanism of MA from a resting-state functional integration point of view.

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Behavioral sensitization induced by methamphetamine causes differential alterations in gene expression and histone acetylation of the prefrontal cortex in rats

Cited by 15 publications

References 55 publications

Epigenetic Regulatory Dynamics in Models of Methamphetamine-Use Disorder

Epigenetic Regulatory Dynamics in Models of Methamphetamine-Use Disorder

Paternal methamphetamine exposure induces higher sensitivity to methamphetamine in male offspring through driving ADRB1 on CaMKII-positive neurons in mPFC

Identification of Methamphetamine Abstainers by Resting-State Functional Magnetic Resonance Imaging

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