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1
Arousal effect of caffeine depends on adenosine A2A receptors in the shell of the nucleus accumbens.咖啡因的觉醒效应取决于伏隔核壳部的腺苷 A2A 受体。
J Neurosci. 2011 Jul 6;31(27):10067-75. doi: 10.1523/JNEUROSCI.6730-10.2011.
2
Adenosine A2A, but not A1, receptors mediate the arousal effect of caffeine.腺苷A2A受体而非A1受体介导咖啡因的兴奋作用。
Nat Neurosci. 2005 Jul;8(7):858-9. doi: 10.1038/nn1491.
3
Physiological roles of A1 and A2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine.利用基因敲除小鼠和咖啡因揭示A1和A2A腺苷受体在调节心率、体温和运动方面的生理作用。
Am J Physiol Heart Circ Physiol. 2009 Apr;296(4):H1141-9. doi: 10.1152/ajpheart.00754.2008. Epub 2009 Feb 13.
4
Opposite modulatory roles for adenosine A1 and A2A receptors on glutamate and dopamine release in the shell of the nucleus accumbens. Effects of chronic caffeine exposure.腺苷A1和A2A受体对伏隔核壳部谷氨酸和多巴胺释放的相反调节作用。长期咖啡因暴露的影响。
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5
Adenosine receptor-mediated modulation of dopamine release in the nucleus accumbens depends on glutamate neurotransmission and N-methyl-D-aspartate receptor stimulation.腺苷受体介导的伏隔核多巴胺释放调节取决于谷氨酸神经传递和N-甲基-D-天冬氨酸受体刺激。
J Neurochem. 2004 Nov;91(4):873-80. doi: 10.1111/j.1471-4159.2004.02761.x.
6
Potentiation of amphetamine-mediated responses in caffeine-sensitized rats involves modifications in A2A receptors and zif-268 mRNAs in striatal neurons.咖啡因致敏大鼠中苯丙胺介导反应的增强涉及纹状体神经元中A2A受体和zif-268 mRNA的改变。
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7
Genetic deletion of GPR52 enhances the locomotor-stimulating effect of an adenosine A receptor antagonist in mice: A potential role of GPR52 in the function of striatopallidal neurons.GPR52基因缺失增强了腺苷A受体拮抗剂对小鼠的运动刺激作用：GPR52在纹状体苍白球神经元功能中的潜在作用
Brain Res. 2017 Sep 1;1670:24-31. doi: 10.1016/j.brainres.2017.05.031. Epub 2017 Jun 3.
8
Absence of quasi-morphine withdrawal syndrome in adenosine A2A receptor knockout mice.腺苷A2A受体基因敲除小鼠中无类似吗啡戒断综合征
Psychopharmacology (Berl). 2006 Apr;185(2):160-8. doi: 10.1007/s00213-005-0284-0. Epub 2006 Feb 10.
9
Caffeine induces dopamine and glutamate release in the shell of the nucleus accumbens.咖啡因会诱导伏隔核壳部释放多巴胺和谷氨酸。
J Neurosci. 2002 Aug 1;22(15):6321-4. doi: 10.1523/JNEUROSCI.22-15-06321.2002.
10
Adenosine A1 and A2A receptors are not upstream of caffeine's dopamine D2 receptor-dependent aversive effects and dopamine-independent rewarding effects.腺苷 A1 和 A2A 受体不是咖啡因多巴胺 D2 受体依赖性厌恶效应和多巴胺非依赖性奖赏效应的上游。
Eur J Neurosci. 2010 Jul;32(1):143-54. doi: 10.1111/j.1460-9568.2010.07247.x. Epub 2010 Jun 22.

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Comparative safety of istradefylline in Parkinson's disease: A systematic review of randomized controlled trials and real-world studies.异他茶碱在帕金森病中的比较安全性：随机对照试验和真实世界研究的系统评价
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本文引用的文献

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The role of adenosine in the regulation of sleep.腺苷在睡眠调节中的作用。
Curr Top Med Chem. 2011;11(8):1047-57. doi: 10.2174/156802611795347654.
2
Sleep state switching.睡眠状态切换。
Neuron. 2010 Dec 22;68(6):1023-42. doi: 10.1016/j.neuron.2010.11.032.
3
Left dorsomedial frontal brain damage is associated with insomnia.左背内侧额前脑损伤与失眠有关。
J Neurosci. 2010 Nov 24;30(47):16041-3. doi: 10.1523/JNEUROSCI.3745-10.2010.
4
Essential role of dopamine D2 receptor in the maintenance of wakefulness, but not in homeostatic regulation of sleep, in mice.多巴胺 D2 受体在维持清醒中的重要作用，但在睡眠的生理性调节中没有作用，在小鼠中。
J Neurosci. 2010 Mar 24;30(12):4382-9. doi: 10.1523/JNEUROSCI.4936-09.2010.
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Cortico-Basal Ganglia reward network: microcircuitry.皮质-基底神经节奖励网络：微电路。
Neuropsychopharmacology. 2010 Jan;35(1):27-47. doi: 10.1038/npp.2009.93.
6
D2R striatopallidal neurons inhibit both locomotor and drug reward processes.D2R 纹状体苍白球神经元抑制运动和药物奖赏过程。
Nat Neurosci. 2009 Apr;12(4):393-5. doi: 10.1038/nn.2286. Epub 2009 Mar 8.
7
Adenosine in the tuberomammillary nucleus inhibits the histaminergic system via A1 receptors and promotes non-rapid eye movement sleep.结节乳头体核中的腺苷通过A1受体抑制组胺能系统，并促进非快速眼动睡眠。
Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19992-7. doi: 10.1073/pnas.0810926105. Epub 2008 Dec 9.
8
Dopaminergic D1 and D2 receptors are essential for the arousal effect of modafinil.多巴胺能D1和D2受体对莫达非尼的觉醒作用至关重要。
J Neurosci. 2008 Aug 20;28(34):8462-9. doi: 10.1523/JNEUROSCI.1819-08.2008.
9
A critical role of the adenosine A2A receptor in extrastriatal neurons in modulating psychomotor activity as revealed by opposite phenotypes of striatum and forebrain A2A receptor knock-outs.纹状体和前脑A2A受体基因敲除小鼠相反的表型揭示了腺苷A2A受体在外纹状体神经元中对调节精神运动活动的关键作用。
J Neurosci. 2008 Mar 19;28(12):2970-5. doi: 10.1523/JNEUROSCI.5255-07.2008.
10
The ventral striatum as an interface between the limbic and motor systems.腹侧纹状体作为边缘系统与运动系统之间的接口。
CNS Spectr. 2007 Dec;12(12):887-92. doi: 10.1017/s1092852900015650.

咖啡因的觉醒效应取决于伏隔核壳部的腺苷 A2A 受体。

Arousal effect of caffeine depends on adenosine A2A receptors in the shell of the nucleus accumbens.

机构信息

Department of Molecular Behavioral Biology, Osaka Bioscience Institute, Suita, Osaka 565-0874, Japan.

出版信息

J Neurosci. 2011 Jul 6;31(27):10067-75. doi: 10.1523/JNEUROSCI.6730-10.2011.

DOI:10.1523/JNEUROSCI.6730-10.2011
PMID:21734299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3153505/
Abstract

Caffeine, the most widely used psychoactive compound, is an adenosine receptor antagonist. It promotes wakefulness by blocking adenosine A(2A) receptors (A(2A)Rs) in the brain, but the specific neurons on which caffeine acts to produce arousal have not been identified. Using selective gene deletion strategies based on the Cre/loxP technology in mice and focal RNA interference to silence the expression of A(2A)Rs in rats by local infection with adeno-associated virus carrying short-hairpin RNA, we report that the A(2A)Rs in the shell region of the nucleus accumbens (NAc) are responsible for the effect of caffeine on wakefulness. Caffeine-induced arousal was not affected in rats when A(2A)Rs were focally removed from the NAc core or other A(2A)R-positive areas of the basal ganglia. Our observations suggest that caffeine promotes arousal by activating pathways that traditionally have been associated with motivational and motor responses in the brain.

摘要

咖啡因是最广泛使用的精神活性化合物，是一种腺苷受体拮抗剂。它通过阻断大脑中的腺苷 A（2A）受体（A（2A）R）来促进觉醒，但尚未确定咖啡因作用于产生觉醒的特定神经元。我们使用基于 Cre/loxP 技术的选择性基因缺失策略，以及通过携带短发夹 RNA 的腺相关病毒局部感染大鼠来沉默 A（2A）R 的表达，报告说，壳核（NAc）的 A（2A）R 负责咖啡因对觉醒的影响。当从 NAc 核心或基底神经节的其他 A（2A）R 阳性区域局部去除 A（2A）R 时，咖啡因引起的觉醒在大鼠中不受影响。我们的观察结果表明，咖啡因通过激活传统上与大脑中的动机和运动反应相关的途径来促进觉醒。