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本文引用的文献

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Serotonin transporter genomic biomarker for quantitative assessment of ondansetron treatment response in alcoholics.用于定量评估酒精成瘾者昂丹司琼治疗反应的5-羟色胺转运体基因组生物标志物。
Front Psychiatry. 2012 Mar 28;3:23. doi: 10.3389/fpsyt.2012.00023. eCollection 2012.
2
The persistence of maladaptive memory: addiction, drug memories and anti-relapse treatments.适应性记忆的持久性:成瘾、药物记忆和抗复发治疗。
Neurosci Biobehav Rev. 2012 Apr;36(4):1119-39. doi: 10.1016/j.neubiorev.2012.01.002. Epub 2012 Jan 24.
3
GABAergic gene expression in postmortem hippocampus from alcoholics and cocaine addicts; corresponding findings in alcohol-naïve P and NP rats.酒精和可卡因成瘾者死后海马 GABA 能基因表达;在酒精未接触的 P 和 NP 大鼠中的相应发现。
PLoS One. 2012;7(1):e29369. doi: 10.1371/journal.pone.0029369. Epub 2012 Jan 13.
4
Central neuropeptide Y modulates binge-like ethanol drinking in C57BL/6J mice via Y1 and Y2 receptors.中枢神经肽 Y 通过 Y1 和 Y2 受体调节 C57BL/6J 小鼠 binge 样乙醇摄入。
Neuropsychopharmacology. 2012 May;37(6):1409-21. doi: 10.1038/npp.2011.327. Epub 2012 Jan 4.
5
The dopamine hypothesis of drug addiction and its potential therapeutic value.药物成瘾的多巴胺假说及其潜在治疗价值。
Front Psychiatry. 2011 Nov 29;2:64. doi: 10.3389/fpsyt.2011.00064. eCollection 2011.
6
Neuropeptide Y (NPY) in the central nucleus of the amygdala (CeA) does not affect ethanol-reinforced responding in binge-drinking, nondependent rats.杏仁中央核(CeA)中的神经肽 Y(NPY)不会影响 binge-drinking、非依赖型大鼠的乙醇强化反应。
Pharmacol Biochem Behav. 2012 Mar;101(1):8-13. doi: 10.1016/j.pbb.2011.11.008. Epub 2011 Nov 18.
7
Novel therapeutic strategies for alcohol and drug addiction: focus on GABA, ion channels and transcranial magnetic stimulation.新型治疗酒精和药物成瘾的策略:聚焦 GABA、离子通道和经颅磁刺激。
Neuropsychopharmacology. 2012 Jan;37(1):163-77. doi: 10.1038/npp.2011.216. Epub 2011 Oct 26.
8
Ethanol increases glutamate neurotransmission in the posterior ventral tegmental area of female wistar rats.乙醇增加雌性 Wistar 大鼠腹侧被盖区后部的谷氨酸神经递质传递。
Alcohol Clin Exp Res. 2012 Apr;36(4):633-40. doi: 10.1111/j.1530-0277.2011.01665.x. Epub 2011 Oct 21.
9
A haplotype analysis is consistent with the role of functional HTR1B variants in alcohol dependence.单体型分析与功能性 HTR1B 变异体在酒精依赖中的作用一致。
Drug Alcohol Depend. 2012 Apr 1;122(1-2):100-4. doi: 10.1016/j.drugalcdep.2011.09.020. Epub 2011 Oct 17.
10
Corticotropin-releasing factor acting on corticotropin-releasing factor receptor type 1 is critical for binge alcohol drinking in mice.促肾上腺皮质激素释放因子作用于促肾上腺皮质激素释放因子受体 1 对于小鼠 binge 饮酒至关重要。
Alcohol Clin Exp Res. 2012 Feb;36(2):369-76. doi: 10.1111/j.1530-0277.2011.01610.x. Epub 2011 Sep 6.

酒精中毒的神经化学和神经结构可塑性。

Neurochemical and neurostructural plasticity in alcoholism.

机构信息

Center for Drug and Alcohol Programs, Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

出版信息

ACS Chem Neurosci. 2012 Jul 18;3(7):494-504. doi: 10.1021/cn300013p. Epub 2012 Apr 16.

DOI:10.1021/cn300013p
PMID:22896799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3419452/
Abstract

The behavioral manifestations of alcoholism are primarily attributable to the numerous and lasting adaptations that occur in the brain as a result of chronic heavy alcohol consumption. As will be reviewed here, these adaptations include alcohol-induced plasticity in chemical neurotransmission, density and morphology of dendritic spines, as well as neurodegeneration and cerebral atrophy. Within the context of these neuroadaptations that have been observed in both human and animal studies, we will discuss how these changes potentially contribute to the cognitive and behavioral dysfunctions that are hallmark features of alcoholism, as well as how they reveal novel potential pharmacological targets for the treatment of this disorder.

摘要

酗酒者的行为表现主要归因于长期大量饮酒导致大脑发生的众多持久适应性变化。正如这里将要回顾的,这些适应性变化包括酒精引起的化学递质传递、树突棘密度和形态的可塑性,以及神经退行性变和脑萎缩。在人类和动物研究中观察到的这些神经适应性变化的背景下,我们将讨论这些变化如何可能导致酒精中毒的认知和行为功能障碍,以及它们如何揭示出治疗这种疾病的新的潜在药理学靶点。