Department of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, PA, USA.
Department of Pharmacology, Penn State College of Medicine, Hershey, PA, USA.
Neuropharmacology. 2018 Sep 1;139:26-40. doi: 10.1016/j.neuropharm.2018.06.037. Epub 2018 Jun 28.
Environmental factors profoundly affect the addictive potential of drugs of abuse and may also modulate the neuro-anatomical/neuro-chemical impacts of uncontrolled drug use and relapse propensity. This study examined the impact of environmental enrichment on heroin self-administration, addiction-related behaviors, and molecular processes proposed to underlie these behaviors. Male Sprague-Dawley rats in standard and enriched housing conditions intravenously self-administered similar amounts of heroin over 14 days. However, environmental enrichment attenuated progressive ratio, extinction, and reinstatement session responding after 14 days of enforced abstinence. Molecular mechanisms, namely DNA methylation and gene expression, are proposed to underlie abstinence-persistent behaviors. A global reduction in methylation is reported to coincide with addiction, but no differences in total genomic methylation or repeat element methylation were observed in CpG or non-CpG (CH) contexts across the mesolimbic circuitry as assessed by multiple methods including whole genome bisulfite sequencing. Immediate early gene expression associated with drug seeking, taking, and abstinence also were examined. EGR1 and EGR2 were suppressed in mesolimbic regions with heroin-taking and environmental enrichment. Site-specific methylation analysis of EGR1 and EGR2 promoter regions using bisulfite amplicon sequencing (BSAS) revealed hypo-methylation in the EGR2 promoter region and EGR1 intragenic CpG sites with heroin-taking and environmental enrichment that was associated with decreased mRNA expression. Taken together, these findings illuminate the impact of drug taking and environment on the epigenome in a locus and gene-specific manner and highlight the need for positive, alternative rewards in the treatment and prevention of drug addiction.
环境因素深刻影响滥用药物的成瘾潜力,也可能调节不受控制的药物使用和复发倾向的神经解剖/神经化学影响。本研究检查了环境丰富对海洛因自我给药、成瘾相关行为以及据推测这些行为基础的分子过程的影响。标准和丰富环境条件下的雄性 Sprague-Dawley 大鼠在 14 天内通过静脉自我给予相似量的海洛因。然而,环境丰富减轻了 14 天强制禁欲后的递增比率、消退和复燃会议反应。据推测,分子机制,即 DNA 甲基化和基因表达,是禁欲持久行为的基础。据报道,与成瘾一致的是,甲基化的全面减少,但在中脑边缘电路中,无论是 CpG 还是非 CpG(CH)背景下,全基因组亚硫酸氢盐测序等多种方法评估的总基因组甲基化或重复元件甲基化均未观察到差异。还检查了与药物寻求、摄取和禁欲相关的即时早期基因表达。海洛因摄取和环境丰富抑制了中脑边缘区域的 EGR1 和 EGR2。使用亚硫酸氢盐扩增子测序 (BSAS) 对 EGR1 和 EGR2 启动子区域进行的特定部位甲基化分析显示,海洛因摄取和环境丰富时 EGR2 启动子区域和 EGR1 内含子 CpG 位点的甲基化减少,这与 mRNA 表达降低有关。总之,这些发现以特定基因和特定基因的方式阐明了药物摄取和环境对表观基因组的影响,并强调了在药物成瘾的治疗和预防中需要积极的替代奖励。