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本文引用的文献

1
Toll-like receptor 4 deficiency alters nucleus accumbens synaptic physiology and drug reward behavior.Toll 样受体 4 缺失改变伏隔核突触生理学和药物奖赏行为。
Proc Natl Acad Sci U S A. 2017 Aug 15;114(33):8865-8870. doi: 10.1073/pnas.1705974114. Epub 2017 Jul 31.
2
Thalamic Regulation of Sucrose Seeking during Unexpected Reward Omission.意外奖励缺失期间丘脑对蔗糖寻求行为的调节
Neuron. 2017 Apr 19;94(2):388-400.e4. doi: 10.1016/j.neuron.2017.03.036.
3
Ventrolateral Striatal Medium Spiny Neurons Positively Regulate Food-Incentive, Goal-Directed Behavior Independently of D1 and D2 Selectivity.腹外侧纹状体中等棘状神经元独立于D1和D2选择性,正向调节食物激励的目标导向行为。
J Neurosci. 2017 Mar 8;37(10):2723-2733. doi: 10.1523/JNEUROSCI.3377-16.2017. Epub 2017 Feb 6.
4
Calcium-permeable AMPA receptors and silent synapses in cocaine-conditioned place preference.可卡因条件性位置偏爱中的钙通透性AMPA受体与沉默突触
EMBO J. 2017 Feb 15;36(4):458-474. doi: 10.15252/embj.201695465. Epub 2017 Jan 11.
5
Pathway- and Cell-Specific Kappa-Opioid Receptor Modulation of Excitation-Inhibition Balance Differentially Gates D1 and D2 Accumbens Neuron Activity.通路和细胞特异性κ-阿片受体对兴奋-抑制平衡的调节以不同方式控制伏隔核D1和D2神经元的活动。
Neuron. 2017 Jan 4;93(1):147-163. doi: 10.1016/j.neuron.2016.12.005.
6
Eating 'Junk-Food' Produces Rapid and Long-Lasting Increases in NAc CP-AMPA Receptors: Implications for Enhanced Cue-Induced Motivation and Food Addiction.食用“垃圾食品”会使伏隔核壳部的CP-AMPA受体迅速且持久增加:对增强线索诱导动机和食物成瘾的影响。
Neuropsychopharmacology. 2016 Dec;41(13):2977-2986. doi: 10.1038/npp.2016.111. Epub 2016 Jul 7.
7
Lack of Specific Involvement of (+)-Naloxone and (+)-Naltrexone on the Reinforcing and Neurochemical Effects of Cocaine and Opioids.(+)-纳洛酮和(+)-纳曲酮对可卡因和阿片类药物强化及神经化学作用无特异性影响。
Neuropsychopharmacology. 2016 Oct;41(11):2772-81. doi: 10.1038/npp.2016.91. Epub 2016 Jun 14.
8
Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function.可卡因体验增强丘脑伏隔核N-甲基-D-天冬氨酸受体功能。
Biol Psychiatry. 2016 Nov 1;80(9):671-681. doi: 10.1016/j.biopsych.2016.04.002. Epub 2016 Apr 7.
9
Microglial TNF-α Suppresses Cocaine-Induced Plasticity and Behavioral Sensitization.小胶质细胞肿瘤坏死因子-α抑制可卡因诱导的可塑性和行为敏化。
Neuron. 2016 May 4;90(3):483-91. doi: 10.1016/j.neuron.2016.03.030. Epub 2016 Apr 21.
10
Cocaine-Induced Synaptic Alterations in Thalamus to Nucleus Accumbens Projection.可卡因诱导的丘脑至伏隔核投射中的突触改变。
Neuropsychopharmacology. 2016 Aug;41(9):2399-410. doi: 10.1038/npp.2016.52. Epub 2016 Apr 14.

伏隔核中的突触可塑性:经验教训。

Synaptic Plasticity in the Nucleus Accumbens: Lessons Learned from Experience.

机构信息

Vanderbilt Brain Institute , Nashville , Tennessee 37232 , United States.

Medical Scientist Training Program , Vanderbilt University School of Medicine , Nashville , Tennessee 37232 , United States.

出版信息

ACS Chem Neurosci. 2018 Sep 19;9(9):2114-2126. doi: 10.1021/acschemneuro.7b00420. Epub 2018 Jan 24.

DOI:10.1021/acschemneuro.7b00420
PMID:29280617
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6508969/
Abstract

Synaptic plasticity contributes to behavioral adaptations. As a key node in the reward pathway, the nucleus accumbens (NAc) is important for determining motivation-to-action outcomes. Across animal models of motivation including addiction, depression, anxiety, and hedonic feeding, selective recruitment of neuromodulatory signals and plasticity mechanisms have been a focus of physiologists and behaviorists alike. Experience-dependent plasticity mechanisms within the NAc vary depending on the distinct afferents and cell-types over time. A greater understanding of molecular mechanisms determining how these changes in synaptic strength track with behavioral adaptations will provide insight into the process of learning and memory along with identifying maladaptations underlying pathological behavior. Here, we summarize recent findings detailing how changes in NAc synaptic strength and mechanisms of plasticity manifest in various models of motivational disorders.

摘要

突触可塑性有助于行为适应。作为奖励通路中的一个关键节点,伏隔核(NAc)对于确定动机与行为结果之间的关系至关重要。在包括成瘾、抑郁、焦虑和享乐性进食在内的各种动机动物模型中,神经调质信号和可塑性机制的选择性募集一直是生理学家和行为学家关注的焦点。NAc 内的经验依赖性可塑性机制随时间的推移而变化,这取决于不同的传入神经和细胞类型。深入了解决定这些突触强度变化如何与行为适应相关的分子机制,将有助于深入了解学习和记忆的过程,并确定病理性行为的适应不良基础。在这里,我们总结了最近的发现,详细说明了 NAc 突触强度变化和可塑性机制在各种动机障碍模型中的表现。