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Consolidating the Circuit Model for Addiction.巩固成瘾的回路模型。
Annu Rev Neurosci. 2021 Jul 8;44:173-195. doi: 10.1146/annurev-neuro-092920-123905. Epub 2021 Mar 5.
2
A non-hallucinogenic psychedelic analogue with therapeutic potential.一种具有治疗潜力的非致幻性迷幻剂类似物。
Nature. 2021 Jan;589(7842):474-479. doi: 10.1038/s41586-020-3008-z. Epub 2020 Dec 9.
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The SERT Met172 Mouse: An Engineered Model To Elucidate the Contributions of Serotonin Signaling to Cocaine Action.SERT Met172 小鼠：阐明血清素信号对可卡因作用贡献的工程化模型。
ACS Chem Neurosci. 2019 Jul 17;10(7):3053-3060. doi: 10.1021/acschemneuro.9b00005. Epub 2019 Mar 13.
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Stochastic synaptic plasticity underlying compulsion in a model of addiction.成瘾模型中强迫行为的随机突触可塑性。
Nature. 2018 Dec;564(7736):366-371. doi: 10.1038/s41586-018-0789-4. Epub 2018 Dec 19.
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Dopamine neurons projecting to medial shell of the nucleus accumbens drive heroin reinforcement.投射到伏隔核内侧壳的多巴胺神经元驱动海洛因强化。
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A transdiagnostic dimensional approach towards a neuropsychological assessment for addiction: an international Delphi consensus study.一种针对成瘾的神经心理学评估的跨诊断维度方法：一项国际 Delphi 共识研究。
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Activation of serotonin neurons promotes active persistence in a probabilistic foraging task.血清素神经元的激活促进在概率性觅食任务中的主动持续行为。
Nat Commun. 2018 Mar 8;9(1):1000. doi: 10.1038/s41467-018-03438-y.
8
Blockade of the 5-HT transporter contributes to the behavioural, neuronal and molecular effects of cocaine.5-羟色胺转运体的阻断作用导致了可卡因的行为、神经元及分子效应。
Br J Pharmacol. 2017 Aug;174(16):2716-2738. doi: 10.1111/bph.13899. Epub 2017 Jul 11.
9
The Emergence of a Circuit Model for Addiction.成瘾的电路模型的出现。
Annu Rev Neurosci. 2016 Jul 8;39:257-76. doi: 10.1146/annurev-neuro-070815-013920. Epub 2016 Apr 21.
10
Sufficiency of Mesolimbic Dopamine Neuron Stimulation for the Progression to Addiction.中脑边缘多巴胺神经元刺激足以导致成瘾。
Neuron. 2015 Dec 2;88(5):1054-1066. doi: 10.1016/j.neuron.2015.10.017. Epub 2015 Nov 12.

5-羟色胺调节可卡因成瘾转变的突触机制。

Synaptic mechanism underlying serotonin modulation of transition to cocaine addiction.

机构信息

Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland.

IDG McGovern Institute for Brain Research, Peking University, Beijing 100871, China.

出版信息

Science. 2021 Sep 10;373(6560):1252-1256. doi: 10.1126/science.abi9086. Epub 2021 Sep 9.

DOI:10.1126/science.abi9086
PMID:34516792
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8817894/
Abstract

Compulsive drug use despite adverse consequences defines addiction. While mesolimbic dopamine signaling is sufficient to drive compulsion, psychostimulants such as cocaine also boost extracellular serotonin (5-HT) by inhibiting reuptake. We used SERT Met172 knockin (SertKI) mice carrying a transporter that no longer binds cocaine to abolish 5-HT transients during drug self-administration. SertKI mice showed an enhanced transition to compulsion. Conversely, pharmacologically elevating 5-HT reversed the inherently high rate of compulsion transition with optogenetic dopamine self-stimulation. The bidirectional effect on behavior is explained by presynaptic depression of orbitofrontal cortex–to–dorsal striatum synapses induced by 5-HT via 5-HT receptors. Consequently, in projection-specific 5-HT receptor knockout mice, the fraction of individuals compulsively self-administering cocaine was elevated.

摘要

尽管存在不良后果，但强迫性药物使用定义了成瘾。虽然中脑边缘多巴胺信号足以驱动强迫，但可卡因等精神兴奋剂通过抑制再摄取来增加细胞外 5-羟色胺 (5-HT)。我们使用携带不再结合可卡因的转运蛋白的 SERT Met172 敲入 (SertKI) 小鼠，在药物自我给药期间消除 5-HT 瞬变。SertKI 小鼠表现出强迫性转变的增强。相反，通过光遗传多巴胺自我刺激，药理学升高 5-HT 逆转了固有高强迫性转变率。这种对行为的双向影响是通过 5-HT 受体介导的 5-HT 引起的眶额皮层到背侧纹状体突触的突触前抑制来解释的。因此，在投射特异性 5-HT 受体敲除小鼠中，强迫性自我给予可卡因的个体比例升高。