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首页> 外文期刊>Behavioral neuroscience >Histone Deacetylase Inhibition Differentially Attenuates Cue-Induced Reinstatement: An Interaction of Environment and acH3K9 Expression in the Dorsal Striatum
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Histone Deacetylase Inhibition Differentially Attenuates Cue-Induced Reinstatement: An Interaction of Environment and acH3K9 Expression in the Dorsal Striatum

机译：组蛋白脱乙酰化酶抑制差异衰减提示诱导的恢复：环境和ACH3K9在背纹体中的相互作用

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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 druginduced 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.
机译：物质使用障碍由复杂的基因环境相互作用驱动。表观遗传组蛋白调节是一种有关药物滥用行为表型的重要因素。仍在调查推动药物吸毒和药物寻求的主要表观遗传机制，目前还不清楚环境条件如何改变表观遗传组酸酯乙酰化，以改变针对药物奖励的行为。该研究检测了环境条件对含疗中的自我管理的影响，以及是否可以通过抑制表观遗传调节剂，组蛋白脱乙酰酶（HDAC）来影响药物吸毒和寻求药物的行为。在富集（EC），隔离（IC）或标准条件（SC）之前饲养30天的雄性大鼠（0.03,0.05,0.1mg / kg /输注，IV）自我给药，消灭和恢复会话。 HDAC抑制剂，Trichostatin A（TSA; 0.3mg / kg，iv）在操作性会话之前注射30分钟。在Amphetamine诱导的恢复（0.25mg / kg，皮下[S.C.]）后，在核心腺（NAC）和背体纹状体（DST）中，提取组织乙酰化组蛋白H3赖氨酸9（ACH3K9）的蛋白质印迹分析。虽然TSA没有显着影响安非他明自我管理或灭绝，但TSA仅减少了Cue，但在IC大鼠中没有粘附恢复。在DST中，但不在NAC中，IC大鼠表现出比EC和SC大鼠显着较低，无论TSA治疗如何。 HDAC抑制降低了在IC大鼠中寻求的愈合症诱导的安非他明醛。虽然IC大鼠在DST中表现得较少，但在DST中表达较少，因此需要进行未来的研究来阐明驱动物质滥用的关键表观因素，特别是在弱势群体中。

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