可卡因诱发腹侧被盖区兴奋性突触传递的突触可塑性。
Cocaine-evoked synaptic plasticity of excitatory transmission in the ventral tegmental area.
机构信息
Department of Basic Neurosciences, University of Geneva, Geneva, Switzerland.
出版信息
Cold Spring Harb Perspect Med. 2013 May 1;3(5):a012013. doi: 10.1101/cshperspect.a012013.
Abstract
Cocaine leads to a strong euphoria, which is at the origin of its recreational use. Past the acute effects, the drug leaves traces in the brain that persist long after it has been cleared from the body. These traces eventually shape behavior such that drug use may become compulsive and addiction develops. Here we discuss cocaine-evoked synaptic plasticity of glutamatergic transmission onto dopamine (DA) neurons of the ventral tegmental area (VTA) as one of the earliest traces after a first injection of cocaine. We review the literature that has examined the induction requirements as well as the expression mechanism of this form of plasticity and ask the question about its functional significance.
摘要
可卡因会引发强烈的欣快感，这也是它被滥用的原因。在急性效应过去后，药物会在大脑中留下痕迹，即使在体内已经清除后仍会持续很长时间。这些痕迹最终会影响行为，导致药物使用变得强迫性，从而产生成瘾。在这里，我们讨论可卡因引发的腹侧被盖区（VTA）中多巴胺（DA）神经元上谷氨酸能传递的突触可塑性，这是首次注射可卡因后最早出现的痕迹之一。我们回顾了检查这种形式可塑性的诱导要求和表达机制的文献，并提出了关于其功能意义的问题。
相似文献
1
Cocaine-evoked synaptic plasticity of excitatory transmission in the ventral tegmental area.可卡因诱发腹侧被盖区兴奋性突触传递的突触可塑性。
Cold Spring Harb Perspect Med. 2013 May 1;3(5):a012013. doi: 10.1101/cshperspect.a012013.
2
Drug-Evoked Synaptic Plasticity of Excitatory Transmission in the Ventral Tegmental Area.药物诱导的腹侧被盖区兴奋性传递的突触可塑性。
Cold Spring Harb Perspect Med. 2021 Apr 1;11(4):a039701. doi: 10.1101/cshperspect.a039701.
3
Cocaine inverts rules for synaptic plasticity of glutamate transmission in the ventral tegmental area.可卡因颠覆了腹侧被盖区谷氨酸传递的突触可塑性规则。
Nat Neurosci. 2011 Apr;14(4):414-6. doi: 10.1038/nn.2763. Epub 2011 Feb 20.
4
Cocaine Exposure Enhances the Activity of Ventral Tegmental Area Dopamine Neurons via Calcium-Impermeable NMDARs.可卡因暴露通过钙不透过性N-甲基-D-天冬氨酸受体增强腹侧被盖区多巴胺能神经元的活性。
J Neurosci. 2016 Oct 19;36(42):10759-10768. doi: 10.1523/JNEUROSCI.1703-16.2016.
5
Acute cocaine exposure alters spine density and long-term potentiation in the ventral tegmental area.急性可卡因暴露会改变腹侧被盖区的树突棘密度和长时程增强效应。
Eur J Neurosci. 2007 Aug;26(3):749-56. doi: 10.1111/j.1460-9568.2007.05689.x.
6
Cocaine-evoked synaptic plasticity: persistence in the VTA triggers adaptations in the NAc.可卡因诱发的突触可塑性：腹侧被盖区的持续性触发伏隔核的适应性变化。
Nat Neurosci. 2009 Aug;12(8):1036-41. doi: 10.1038/nn.2367. Epub 2009 Jul 13.
7
Cocaine Selectively Reorganizes Excitatory Inputs to Substantia Nigra Pars Compacta Dopamine Neurons.可卡因选择性重塑中脑腹侧被盖区多巴胺神经元的兴奋性输入。
J Neurosci. 2018 Jan 31;38(5):1151-1159. doi: 10.1523/JNEUROSCI.1975-17.2017. Epub 2017 Dec 20.
8
Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine.慢性可卡因处理后腹侧被盖区的突触和内在可塑性。
Curr Opin Neurobiol. 2019 Feb;54:66-72. doi: 10.1016/j.conb.2018.08.013. Epub 2018 Sep 17.
9
Inactivation of NMDA Receptors in the Ventral Tegmental Area during Cocaine Self-Administration Prevents GluA1 Upregulation but with Paradoxical Increases in Cocaine-Seeking Behavior.在可卡因自我给药期间，腹侧被盖区 NMDA 受体的失活可阻止 GluA1 的上调，但可卡因觅药行为却出现反常增加。
J Neurosci. 2018 Jan 17;38(3):575-585. doi: 10.1523/JNEUROSCI.2828-16.2017. Epub 2017 Dec 1.
10
Expression of cocaine-evoked synaptic plasticity by GluN3A-containing NMDA receptors.表达可卡因诱导的突触可塑性由含 GluN3A 的 NMDA 受体。
Neuron. 2013 Nov 20;80(4):1025-38. doi: 10.1016/j.neuron.2013.07.050. Epub 2013 Oct 31.
引用本文的文献
1
Calcium-permeable AMPA receptor activity and GluA1 trafficking in the basolateral amygdala regulate operant alcohol self-administration.在基底外侧杏仁核中，钙通透性 AMPA 受体活性和 GluA1 转运调节操作性酒精自我给药。
Addict Biol. 2021 Sep;26(5):e13049. doi: 10.1111/adb.13049. Epub 2021 May 5.
2
Single Exposure to Cocaine Impairs Reinforcement Learning by Potentiating the Activity of Neurons in the Direct Striatal Pathway in Mice.单次可卡因暴露通过增强小鼠直接纹状体通路神经元的活性来损害强化学习。
Neurosci Bull. 2021 Aug;37(8):1119-1134. doi: 10.1007/s12264-021-00687-8. Epub 2021 Apr 27.
3
Acute cocaine exposure occludes long-term depression in ventral tegmental area GABA neurons.急性可卡因暴露阻断腹侧被盖区 GABA 神经元的长时程抑郁。
Neurochem Int. 2021 May;145:105002. doi: 10.1016/j.neuint.2021.105002. Epub 2021 Feb 20.
4
Alpha-1 Adrenergic Receptors Modulate Glutamate and GABA Neurotransmission onto Ventral Tegmental Dopamine Neurons during Cocaine Sensitization.α1 肾上腺素能受体在可卡因敏化过程中调节腹侧被盖区多巴胺神经元上的谷氨酸和 GABA 神经传递。
Int J Mol Sci. 2020 Jan 25;21(3):790. doi: 10.3390/ijms21030790.
5
Structural and Functional Alterations in Betel-Quid Chewers: A Systematic Review of Neuroimaging Findings.嚼槟榔者的结构和功能改变：神经影像学研究结果的系统评价
Front Psychiatry. 2019 Jan 29;10:16. doi: 10.3389/fpsyt.2019.00016. eCollection 2019.
6
Emergence of Endocytosis-Dependent mGlu1 LTD at Nucleus Accumbens Synapses After Withdrawal From Cocaine Self-Administration.可卡因自我给药戒断后伏隔核突触处内吞作用依赖性代谢型谷氨酸受体1长时程抑制的出现。
Front Synaptic Neurosci. 2018 Oct 23;10:36. doi: 10.3389/fnsyn.2018.00036. eCollection 2018.
7
Granulocyte-Colony-Stimulating Factor Alters the Proteomic Landscape of the Ventral Tegmental Area.粒细胞集落刺激因子改变腹侧被盖区的蛋白质组格局。
Proteomes. 2018 Sep 23;6(4):35. doi: 10.3390/proteomes6040035.
8
Cocaine Effects on Dopaminergic Transmission Depend on a Balance between Sigma-1 and Sigma-2 Receptor Expression.可卡因对多巴胺能传递的影响取决于西格玛-1和西格玛-2受体表达之间的平衡。
Front Mol Neurosci. 2018 Feb 12;11:17. doi: 10.3389/fnmol.2018.00017. eCollection 2018.
9
Glutamate Transport: A New Bench to Bedside Mechanism for Treating Drug Abuse.谷氨酸转运：治疗药物滥用的新的基础到临床机制。
Int J Neuropsychopharmacol. 2017 Oct 1;20(10):797-812. doi: 10.1093/ijnp/pyx050.
10
Cadherins mediate cocaine-induced synaptic plasticity and behavioral conditioning.钙黏着蛋白介导可卡因诱导的突触可塑性和行为条件反射。
Nat Neurosci. 2017 Apr;20(4):540-549. doi: 10.1038/nn.4503. Epub 2017 Feb 13.
本文引用的文献
1
Activation of VTA GABA neurons disrupts reward consumption.腹侧被盖区 GABA 神经元的激活会破坏奖赏性消费。
Neuron. 2012 Mar 22;73(6):1184-94. doi: 10.1016/j.neuron.2012.02.016. Epub 2012 Mar 21.
2
GABA neurons of the VTA drive conditioned place aversion.腹侧被盖区的 GABA 神经元驱动条件性位置厌恶。
Neuron. 2012 Mar 22;73(6):1173-83. doi: 10.1016/j.neuron.2012.02.015. Epub 2012 Mar 21.
3
Protein kinase mζ is necessary for cocaine-induced synaptic potentiation in the ventral tegmental area.蛋白激酶 mζ 对于伏隔核内可卡因诱导的突触强化是必要的。
Biol Psychiatry. 2012 Apr 15;71(8):706-13. doi: 10.1016/j.biopsych.2011.10.031. Epub 2011 Dec 9.
4
Group I mGluR activation reverses cocaine-induced accumulation of calcium-permeable AMPA receptors in nucleus accumbens synapses via a protein kinase C-dependent mechanism.I 型代谢型谷氨酸受体的激活通过蛋白激酶 C 依赖的机制逆转可卡因诱导的伏隔核突触中钙通透性 AMPA 受体的积累。
J Neurosci. 2011 Oct 12;31(41):14536-41. doi: 10.1523/JNEUROSCI.3625-11.2011.
5
In utero exposure to cocaine delays postnatal synaptic maturation of glutamatergic transmission in the VTA.可卡因宫内暴露延迟 VTA 中谷氨酸能传递的产后突触成熟。
Nat Neurosci. 2011 Oct 2;14(11):1439-46. doi: 10.1038/nn.2930.
6
Projection-specific modulation of dopamine neuron synapses by aversive and rewarding stimuli.厌恶刺激和奖赏刺激对多巴胺神经元突触的特异性投射调节。
Neuron. 2011 Jun 9;70(5):855-62. doi: 10.1016/j.neuron.2011.03.025.
7
Nicotine potentiation of excitatory inputs to ventral tegmental area dopamine neurons.尼古丁增强腹侧被盖区多巴胺神经元的兴奋性输入。
J Neurosci. 2011 May 4;31(18):6710-20. doi: 10.1523/JNEUROSCI.5671-10.2011.
8
Molecular basis of NMDA receptor functional diversity.NMDA 受体功能多样性的分子基础。
Eur J Neurosci. 2011 Apr;33(8):1351-65. doi: 10.1111/j.1460-9568.2011.07628.x. Epub 2011 Mar 14.
9
Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling.药物诱发的成瘾性突触可塑性：从分子变化到回路重塑。
Neuron. 2011 Feb 24;69(4):650-63. doi: 10.1016/j.neuron.2011.01.017.
10
How addictive drugs disrupt presynaptic dopamine neurotransmission.药物成瘾如何破坏突触前多巴胺递质传递。
Neuron. 2011 Feb 24;69(4):628-49. doi: 10.1016/j.neuron.2011.02.010.
Zotero 插件