安非他命的表观遗传机制。
The Epigenetic Mechanisms of Amphetamine.
作者信息
McCowan Talus J, Dhasarathy Archana, Carvelli Lucia
机构信息
Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA.
出版信息
J Addict Prev. 2015;2015(Suppl 1). doi: 10.13188/2330-2178.S100001. Epub 2015 Feb 9.
Abstract
Amphetamine (AMPH) is a psychostimulant and the most prescribed drug to treat attention deficit hyperactive disorder (ADHD). Although therapeutically used doses are generally well tolerated, numerous side effects are still known to occur, such as jitteriness, loss of appetite and psychosis. Moreover, AMPH is liable to be abused by users looking for increased alertness, weight loss or athletic performance. A growing body of evidence indicates that drugs of abuse, including AMPH, control gene expression through chromatin modifications. However, while numerous studies have investigated the molecular mechanisms of AMPH action, only a small number of studies have explored changes in gene expression caused by AMPH. This review examines the epigenetic changes induced by chronic and acute treatments with AMPH and includes, where relevant, data obtained with other psychostimulants such as methamphetamine and cocaine.
摘要
苯丙胺（AMPH）是一种精神兴奋剂，也是治疗注意力缺陷多动障碍（ADHD）最常用的处方药。虽然治疗剂量通常耐受性良好，但仍已知会出现许多副作用，如神经过敏、食欲不振和精神病。此外，AMPH容易被寻求提高警觉性、减肥或提高运动表现的使用者滥用。越来越多的证据表明，包括AMPH在内的滥用药物通过染色质修饰来控制基因表达。然而，虽然许多研究调查了AMPH作用的分子机制，但只有少数研究探索了AMPH引起的基因表达变化。本综述研究了AMPH慢性和急性治疗引起的表观遗传变化，并在相关情况下纳入了用其他精神兴奋剂如甲基苯丙胺和可卡因获得的数据。
相似文献
1
The Epigenetic Mechanisms of Amphetamine.安非他命的表观遗传机制。
J Addict Prev. 2015;2015(Suppl 1). doi: 10.13188/2330-2178.S100001. Epub 2015 Feb 9.
2
Neurochemical and behavioral differences between d-methamphetamine and d-amphetamine in rats.大鼠中右旋甲基苯丙胺和右旋苯丙胺之间的神经化学及行为差异
Psychopharmacology (Berl). 2003 Feb;165(4):359-69. doi: 10.1007/s00213-002-1288-7. Epub 2002 Dec 19.
3
The Efficacy and Safety of Evekeo, Racemic Amphetamine Sulfate, for Treatment of Attention-Deficit/Hyperactivity Disorder Symptoms: A Multicenter, Dose-Optimized, Double-Blind, Randomized, Placebo-Controlled Crossover Laboratory Classroom Study.硫酸右苯丙胺（Evekeo）治疗注意力缺陷/多动障碍症状的疗效与安全性：一项多中心、剂量优化、双盲、随机、安慰剂对照的交叉实验室课堂研究。
J Child Adolesc Psychopharmacol. 2015 Jun;25(5):402-14. doi: 10.1089/cap.2014.0176. Epub 2015 Feb 18.
4
Different effects of behaviorally equipotent doses of amphetamine and methamphetamine on brain biogenic amines: specific increase of phenylethylamine by amphetamine.苯丙胺和甲基苯丙胺行为等效剂量对脑内生物胺的不同影响：苯丙胺使苯乙胺特异性增加。
Eur J Pharmacol. 1982 Jul 16;81(3):385-92. doi: 10.1016/0014-2999(82)90103-0.
5
Exposure to methylphenidate in adolescence and adulthood modulates cross-sensitization to amphetamine in adulthood in three genetically variant female rat strains.在三种基因变异的雌性大鼠品系中，青春期和成年期接触哌甲酯会调节成年期对苯丙胺的交叉致敏作用。
Behav Brain Res. 2019 Apr 19;362:36-45. doi: 10.1016/j.bbr.2018.12.018. Epub 2018 Dec 14.
6
Early-Onset Efficacy and Safety Pilot Study of Amphetamine Extended-Release Oral Suspension in the Treatment of Children with Attention-Deficit/Hyperactivity Disorder.苯丙胺缓释口服混悬液治疗儿童注意缺陷多动障碍的早期疗效与安全性初步研究
J Child Adolesc Psychopharmacol. 2019 Feb;29(1):2-8. doi: 10.1089/cap.2018.0078. Epub 2018 Dec 21.
7
Adolescent exposure to cocaine, amphetamine, and methylphenidate cross-sensitizes adults to methamphetamine with drug- and sex-specific effects.青少年接触可卡因、苯丙胺和哌醋甲酯会使成年人对甲基苯丙胺产生交叉敏感，且存在药物和性别特异性影响。
Behav Brain Res. 2015 Mar 15;281:116-24. doi: 10.1016/j.bbr.2014.12.002. Epub 2014 Dec 8.
8
A threshold neurotoxic amphetamine exposure inhibits parietal cortex expression of synaptic plasticity-related genes.阈下神经毒性苯丙胺暴露会抑制顶叶皮质中突触可塑性相关基因的表达。
Neuroscience. 2007 Jan 5;144(1):66-76. doi: 10.1016/j.neuroscience.2006.08.076. Epub 2006 Oct 13.
9
The effects of amphetamine exposure on juvenile rats on the neuronal morphology of the limbic system at prepubertal, pubertal and postpubertal ages.苯丙胺暴露对青春期前、青春期和青春期后幼鼠边缘系统神经元形态的影响。
J Chem Neuroanat. 2016 Nov;77:68-77. doi: 10.1016/j.jchemneu.2016.05.004. Epub 2016 May 18.
10
Paradoxical effects of D-amphetamine in infant and adolescent mice: role of gender and environmental risk factors.
Neurosci Biobehav Rev. 2000 Jan;24(1):73-84. doi: 10.1016/s0149-7634(99)00047-0.
引用本文的文献
1
How life events may confer vulnerability to addiction: the role of epigenetics.生活事件如何使人易患成瘾症：表观遗传学的作用。
Front Mol Neurosci. 2024 Sep 18;17:1462769. doi: 10.3389/fnmol.2024.1462769. eCollection 2024.
2
Substance-Induced Psychiatric Disorders, Epigenetic and Microbiome Alterations, and Potential for Therapeutic Interventions.物质所致精神障碍、表观遗传和微生物组改变以及治疗干预的潜力。
Brain Sci. 2024 Jul 30;14(8):769. doi: 10.3390/brainsci14080769.
3
Amphetamine exposure during embryogenesis changes expression and function of the dopamine transporter in Caenorhabditis elegans offspring.胚胎发育期接触苯丙胺会改变秀丽隐杆线虫后代中多巴胺转运体的表达和功能。
J Neurochem. 2024 Sep;168(9):2989-2998. doi: 10.1111/jnc.16166. Epub 2024 Jul 3.
4
Therapeutic Use and Chronic Abuse of CNS Stimulants and Anabolic Drugs.中枢神经系统兴奋剂和合成代谢药物的治疗用途及长期滥用
Curr Issues Mol Biol. 2022 Oct 15;44(10):4902-4920. doi: 10.3390/cimb44100333.
5
The Role of Epigenetics in the Pathogenesis and Potential Treatment of Attention Deficit Hyperactivity Disorder.表观遗传学在注意缺陷多动障碍发病机制及潜在治疗中的作用。
Curr Neuropharmacol. 2022 Aug 3;20(9):1642-1650. doi: 10.2174/1570159X19666210920091036.
6
Histone deacetylase inhibition differentially attenuates cue-induced reinstatement: An interaction of environment and acH3K9 expression in the dorsal striatum.组蛋白去乙酰化酶抑制作用对线索诱导的复吸有不同程度的减弱：背侧纹状体中环境与乙酰化组蛋白H3赖氨酸9表达的相互作用。
Behav Neurosci. 2019 Oct;133(5):478-488. doi: 10.1037/bne0000333. Epub 2019 Jul 25.
7
Epigenetic profiling of ADHD symptoms trajectories: a prospective, methylome-wide study.注意缺陷多动障碍症状轨迹的表观遗传学分析：一项前瞻性全甲基化组研究。
Mol Psychiatry. 2017 Feb;22(2):250-256. doi: 10.1038/mp.2016.85. Epub 2016 May 24.
8
Current and Future Prospects for Epigenetic Biomarkers of Substance Use Disorders.物质使用障碍的表观遗传生物标志物的现状和未来前景。
Genes (Basel). 2015 Oct 14;6(4):991-1022. doi: 10.3390/genes6040991.
本文引用的文献
1
Locus-specific epigenetic remodeling controls addiction- and depression-related behaviors.特定基因座的表观遗传重塑控制成瘾和抑郁相关行为。
Nat Neurosci. 2014 Dec;17(12):1720-7. doi: 10.1038/nn.3871. Epub 2014 Oct 27.
2
Elevated 5-hydroxymethylcytosine in the Engrailed-2 (EN-2) promoter is associated with increased gene expression and decreased MeCP2 binding in autism cerebellum.在自闭症患者的小脑组织中，Engrailed-2（EN-2）启动子区域5-羟甲基胞嘧啶水平升高与基因表达增加及MeCP2结合减少相关。
Transl Psychiatry. 2014 Oct 7;4(10):e460. doi: 10.1038/tp.2014.87.
3
Chronic cocaine-regulated epigenomic changes in mouse nucleus accumbens.慢性可卡因对小鼠伏隔核表观基因组的调控变化
Genome Biol. 2014 Apr 22;15(4):R65. doi: 10.1186/gb-2014-15-4-r65.
4
Long-term parental methamphetamine exposure of mice influences behavior and hippocampal DNA methylation of the offspring.长期暴露于父母的冰毒会影响后代的行为和海马体 DNA 甲基化。
Mol Psychiatry. 2015 Feb;20(2):232-9. doi: 10.1038/mp.2014.7. Epub 2014 Feb 18.
5
Increased binding of MeCP2 to the GAD1 and RELN promoters may be mediated by an enrichment of 5-hmC in autism spectrum disorder (ASD) cerebellum.在自闭症谱系障碍（ASD）小脑组织中，5-羟甲基胞嘧啶（5-hmC）水平的升高可能介导了MeCP2与谷氨酸脱羧酶1（GAD1）和Reelin（RELN）启动子结合的增加。
Transl Psychiatry. 2014 Jan 21;4(1):e349. doi: 10.1038/tp.2013.123.
6
Changes in microRNA expression profile in hippocampus during the acquisition and extinction of cocaine-induced conditioned place preference in rats.在大鼠可卡因诱导的条件性位置偏爱获得和消退过程中海马中 microRNA 表达谱的变化。
J Biomed Sci. 2013 Dec 20;20(1):96. doi: 10.1186/1423-0127-20-96.
7
Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania.躁狂症药理学模型中的组蛋白去乙酰化酶活性和脑源性神经营养因子（BDNF）水平。
Braz J Psychiatry. 2014 Jan-Mar;36(1):39-46. doi: 10.1590/1516-4446-2013-1094. Epub 2013 Dec 10.
8
Persistent gene expression changes in NAc, mPFC, and OFC associated with previous nicotine or amphetamine exposure.与先前尼古丁或安非他命暴露相关的 NAc、mPFC 和 OFC 中持续的基因表达变化。
Behav Brain Res. 2013 Nov 1;256:655-61. doi: 10.1016/j.bbr.2013.09.006. Epub 2013 Sep 7.
9
A selective HDAC 1/2 inhibitor modulates chromatin and gene expression in brain and alters mouse behavior in two mood-related tests.一种选择性的 HDAC1/2 抑制剂可调节大脑中的染色质和基因表达，并改变两种与情绪相关的小鼠行为测试中的小鼠行为。
PLoS One. 2013 Aug 14;8(8):e71323. doi: 10.1371/journal.pone.0071323. eCollection 2013.
10
Sodium butyrate reverses the inhibition of Krebs cycle enzymes induced by amphetamine in the rat brain.丁酸钠可逆转安非他命诱导的大鼠脑组织三羧酸循环酶的抑制。
J Neural Transm (Vienna). 2013 Dec;120(12):1737-42. doi: 10.1007/s00702-013-1056-3. Epub 2013 Jul 14.
Zotero 插件