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可卡因诱导的谷氨酸传递神经适应:对渴望和成瘾的潜在治疗靶点。

Cocaine-induced neuroadaptations in glutamate transmission: potential therapeutic targets for craving and addiction.

机构信息

Department of Psychiatry, Center for Neurobiology and Behavior, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

出版信息

Ann N Y Acad Sci. 2010 Feb;1187:35-75. doi: 10.1111/j.1749-6632.2009.05144.x.

DOI:10.1111/j.1749-6632.2009.05144.x
PMID:20201846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5413205/
Abstract

A growing body of evidence indicates that repeated exposure to cocaine leads to profound changes in glutamate transmission in limbic nuclei, particularly the nucleus accumbens. This review focuses on preclinical studies of cocaine-induced behavioral plasticity, including behavioral sensitization, self-administration, and the reinstatement of cocaine seeking. Behavioral, pharmacological, neurochemical, electrophysiological, biochemical, and molecular biological changes associated with cocaine-induced plasticity in glutamate systems are reviewed. The ultimate goal of these lines of research is to identify novel targets for the development of therapies for cocaine craving and addiction. Therefore, we also outline the progress and prospects of glutamate modulators for the treatment of cocaine addiction.

摘要

越来越多的证据表明,反复接触可卡因会导致边缘核(尤其是伏隔核)中谷氨酸传递的深刻变化。这篇综述重点介绍了可卡因引起的行为可塑性的临床前研究,包括行为敏感化、自我给药和可卡因寻求的恢复。本文综述了与可卡因诱导的谷氨酸系统可塑性相关的行为、药理学、神经化学、电生理学、生物化学和分子生物学变化。这些研究的最终目标是确定开发可卡因渴望和成瘾治疗方法的新靶点。因此,我们还概述了谷氨酸调节剂治疗可卡因成瘾的进展和前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/012e5d25b6cf/nihms856306f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/78bc832ba552/nihms856306f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/c3499f0647dd/nihms856306f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/012e5d25b6cf/nihms856306f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/78bc832ba552/nihms856306f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/c3499f0647dd/nihms856306f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e4a/5413205/012e5d25b6cf/nihms856306f3.jpg

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本文引用的文献

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Metabotropic glutamate receptor 5 (mGluR5) antagonists attenuate cocaine priming- and cue-induced reinstatement of cocaine seeking.代谢型谷氨酸受体5(mGluR5)拮抗剂可减弱可卡因引发及线索诱导的可卡因觅求复燃。
Behav Brain Res. 2009 Sep 14;202(2):238-44. doi: 10.1016/j.bbr.2009.03.039. Epub 2009 Apr 5.
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D-cycloserine accelerates the extinction of cocaine-induced conditioned place preference in C57bL/c mice.D-环丝氨酸可加速C57bL/c小鼠中可卡因诱导的条件性位置偏好的消退。
Behav Brain Res. 2009 May 16;199(2):345-9. doi: 10.1016/j.bbr.2008.12.025. Epub 2008 Dec 30.
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D-cycloserine potentiates the reconsolidation of cocaine-associated memories.D-环丝氨酸增强可卡因相关记忆的重新巩固。
Learn Mem. 2009 Jan 7;16(1):82-5. doi: 10.1101/lm.1186609. Print 2009 Jan.
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N-Acetylcysteine reverses cocaine-induced metaplasticity.N-乙酰半胱氨酸可逆转可卡因诱导的可塑性变化。
Nat Neurosci. 2009 Feb;12(2):182-9. doi: 10.1038/nn.2250. Epub 2009 Jan 11.
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The preferential dopamine D3 receptor antagonist S33138 inhibits cocaine reward and cocaine-triggered relapse to drug-seeking behavior in rats.选择性多巴胺D3受体拮抗剂S33138可抑制大鼠的可卡因奖赏效应以及可卡因引发的觅药行为复燃。
Neuropharmacology. 2009 Mar;56(4):752-60. doi: 10.1016/j.neuropharm.2008.12.007.
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Glutamate: the new frontier in pharmacotherapy for cocaine addiction.谷氨酸:可卡因成瘾药物治疗的新前沿。
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7
Neuroadaptations in the cellular and postsynaptic group 1 metabotropic glutamate receptor mGluR5 and Homer proteins following extinction of cocaine self-administration.可卡因自我给药消退后,细胞和突触后第1组代谢型谷氨酸受体mGluR5及荷马蛋白的神经适应性变化。
Neurosci Lett. 2009 Mar 13;452(2):167-71. doi: 10.1016/j.neulet.2008.12.028. Epub 2008 Dec 24.
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Behavioral sensitization to cocaine is associated with increased glutamate receptor trafficking to the postsynaptic density after extended withdrawal period.对可卡因的行为敏化与延长戒断期后谷氨酸受体向突触后致密区的转运增加有关。
Neuroscience. 2009 Mar 3;159(1):414-26. doi: 10.1016/j.neuroscience.2008.10.027. Epub 2008 Nov 1.
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The role of cystine-glutamate exchange in nicotine dependence in rats and humans.胱氨酸-谷氨酸交换在大鼠和人类尼古丁依赖中的作用。
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Sex differences in basal and cocaine-induced alterations in PKA and CREB proteins in the nucleus accumbens.伏隔核中蛋白激酶A(PKA)和环磷腺苷效应元件结合蛋白(CREB)在基础状态及可卡因诱导下的变化中的性别差异。
Psychopharmacology (Berl). 2009 Apr;203(3):641-50. doi: 10.1007/s00213-008-1411-5. Epub 2008 Dec 4.