Arndt David L, Wukitsch Thomas J, Garcia Erik J, Cain Mary
Department of Psychological Sciences.
Behav Neurosci. 2019 Oct;133(5):478-488. doi: 10.1037/bne0000333. Epub 2019 Jul 25.
Substance use disorder is driven by complex gene-environment interactions. Epigenetic histone regulation is a significant contributor to several behavioral phenotypes of drug abuse. The primary epigenetic mechanisms that drive drug taking and drug seeking are still being investigated, and it is unclear how environmental conditions alter epigenetic histone acetylation to change behaviors geared toward drug reward. This study examined the effects of environmental condition on amphetamine self-administration, and whether drug-taking and drug-seeking behaviors could be influenced through inhibition of an epigenetic regulator, histone deacetylase (HDAC). Male rats reared for 30 days in enriched (EC), isolated (IC), or standard conditions (SC) prior to amphetamine (0.03, 0.05, 0.1 mg/kg/infusion, IV) self-administration, extinction, and reinstatement sessions. The HDAC inhibitor, Trichostatin A (TsA; 0.3 mg/kg, IV), was injected 30 min prior to operant sessions. After amphetamine-induced reinstatement (0.25 mg/kg, subcutaneous [s.c.]), tissue was extracted for Western blot analyses of acetylated histone H3 lysine 9 (acH3K9) in the nucleus accumbens (NAc) and dorsal striatum (DSt). While TsA did not significantly affect amphetamine self-administration or extinction, TsA decreased cue-, but not drug-induced reinstatement in IC rats only. In the DSt, but not in the NAc, IC rats exhibited significantly less acH3K9 expression than EC and SC rats, irrespective of TsA treatment. HDAC inhibition decreases cue-induced reinstatement of amphetamine seeking in IC rats. While IC rats exhibit less acH3K9 expression in the DSt, future studies are needed to elucidate the critical epigenetic factors that drive substance abuse, particularly in vulnerable populations. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
物质使用障碍是由复杂的基因 - 环境相互作用驱动的。表观遗传组蛋白调控是药物滥用的几种行为表型的重要促成因素。驱动药物摄取和觅药行为的主要表观遗传机制仍在研究中,目前尚不清楚环境条件如何改变表观遗传组蛋白乙酰化以改变与药物奖赏相关的行为。本研究考察了环境条件对苯丙胺自我给药的影响,以及药物摄取和觅药行为是否可通过抑制一种表观遗传调节因子组蛋白去乙酰化酶(HDAC)而受到影响。雄性大鼠在进行苯丙胺(0.03、0.05、0.1mg/kg/输注,静脉注射)自我给药、消退和复吸实验之前,先在丰富环境(EC)、隔离环境(IC)或标准环境(SC)中饲养30天。在操作性实验前30分钟注射HDAC抑制剂曲古抑菌素A(TsA;0.3mg/kg,静脉注射)。在苯丙胺诱导的复吸(0.25mg/kg,皮下注射)后,提取组织用于伏隔核(NAc)和背侧纹状体(DSt)中乙酰化组蛋白H3赖氨酸9(acH3K9)的蛋白质印迹分析。虽然TsA对苯丙胺自我给药或消退没有显著影响,但TsA仅降低了IC大鼠由线索诱导而非药物诱导的复吸。在DSt而非NAc中,无论TsA处理如何,IC大鼠的acH3K9表达均显著低于EC和SC大鼠。HDAC抑制降低了IC大鼠中由线索诱导的苯丙胺觅药行为的复吸。虽然IC大鼠在DSt中表现出较低的acH3K9表达,但未来仍需要研究来阐明驱动物质滥用的关键表观遗传因素,特别是在易感人群中。(PsycINFO数据库记录(c)2019美国心理学会,保留所有权利)