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Neutral antagonist activity of naltrexone and 6beta-naltrexol in naïve and opioid-dependent C6 cells expressing a mu-opioid receptor.纳曲酮和6β-纳曲醇在表达μ阿片受体的未接触过阿片类药物及阿片类药物依赖的C6细胞中的中性拮抗活性。
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Chronic exposure to mu-opioid agonists produces constitutive activation of mu-opioid receptors in direct proportion to the efficacy of the agonist used for pretreatment.长期暴露于μ-阿片受体激动剂会导致μ-阿片受体的组成性激活,其激活程度与用于预处理的激动剂的效力成正比。
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Neutral antagonist activity of naltrexone and 6beta-naltrexol in naïve and opioid-dependent C6 cells expressing a mu-opioid receptor.纳曲酮和6β-纳曲醇在表达μ阿片受体的未接触过阿片类药物及阿片类药物依赖的C6细胞中的中性拮抗活性。
Br J Pharmacol. 2009 Apr;156(7):1044-53. doi: 10.1111/j.1476-5381.2008.00035.x. Epub 2009 Feb 13.
2
Comparison of the opioid receptor antagonist properties of naltrexone and 6 beta-naltrexol in morphine-naïve and morphine-dependent mice.纳曲酮和6β-纳曲醇对未使用过吗啡及吗啡依赖小鼠阿片受体拮抗特性的比较。
Eur J Pharmacol. 2008 Mar 31;583(1):48-55. doi: 10.1016/j.ejphar.2008.01.004. Epub 2008 Jan 24.
3
Comparison of naltrexone, 6alpha-naltrexol, and 6beta-naltrexol in morphine-dependent and in nondependent rhesus monkeys.纳曲酮、6α-纳曲醇和6β-纳曲醇在吗啡依赖和非依赖恒河猴中的比较。
Psychopharmacology (Berl). 2008 Jan;195(4):479-86. doi: 10.1007/s00213-007-0914-9. Epub 2007 Sep 16.
4
Mu-opioid receptor up-regulation and functional supersensitivity are independent of antagonist efficacy.μ-阿片受体上调和功能超敏性与拮抗剂效能无关。
J Pharmacol Exp Ther. 2007 Nov;323(2):701-7. doi: 10.1124/jpet.107.127019. Epub 2007 Aug 14.
5
In vivo characterization of 6beta-naltrexol, an opioid ligand with less inverse agonist activity compared with naltrexone and naloxone in opioid-dependent mice.6β-纳曲醇在体内的特性研究,该阿片类配体在阿片类药物依赖小鼠中的反向激动活性低于纳曲酮和纳洛酮。
J Pharmacol Exp Ther. 2005 Jun;313(3):1150-62. doi: 10.1124/jpet.104.082966. Epub 2005 Feb 16.
6
Basal opioid receptor activity, neutral antagonists, and therapeutic opportunities.基础阿片受体活性、中性拮抗剂与治疗机会。
Life Sci. 2005 Feb 11;76(13):1427-37. doi: 10.1016/j.lfs.2004.10.024. Epub 2004 Dec 8.
7
Efficacy as a vector: the relative prevalence and paucity of inverse agonism.作为载体的功效:反向激动作用的相对发生率和稀缺性。
Mol Pharmacol. 2004 Jan;65(1):2-11. doi: 10.1124/mol.65.1.2.
8
Basal signaling activity of mu opioid receptor in mouse brain: role in narcotic dependence.小鼠脑中μ阿片受体的基础信号活性:在麻醉依赖性中的作用。
J Pharmacol Exp Ther. 2004 Feb;308(2):512-20. doi: 10.1124/jpet.103.054049. Epub 2003 Nov 4.
9
Effects of morphine withdrawal on micro-opioid receptor-stimulated guanylyl 5'-[gamma-[35S]thio]-triphosphate autoradiography in rat brain.吗啡戒断对大鼠脑内微阿片受体刺激的鸟苷酰5'-[γ-[35S]硫代]-三磷酸放射自显影的影响。
Eur J Pharmacol. 2002 Jun 20;446(1-3):43-51. doi: 10.1016/s0014-2999(02)01763-6.
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Enhanced opioid efficacy in opioid dependence is caused by an altered signal transduction pathway.阿片类药物依赖中增强的阿片类药物疗效是由信号转导途径改变所致。
J Neurosci. 1998 Dec 15;18(24):10269-76. doi: 10.1523/JNEUROSCI.18-24-10269.1998.

μ星上的阴影?重新审视组成型活性μ阿片受体。

Shadows across mu-Star? Constitutively active mu-opioid receptors revisited.

作者信息

Connor Mark

机构信息

Pain Management Research Institute, Kolling Institute, University of Sydney at Royal North Hospital St Leonards, 100 Mallet Street, Camperdown, NSW 2050, Australia.

出版信息

Br J Pharmacol. 2009 Apr;156(7):1041-3. doi: 10.1111/j.1476-5381.2009.00067.x.

DOI:10.1111/j.1476-5381.2009.00067.x
PMID:19368530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2697690/
Abstract

Constitutively active mu-opioid receptors (mu* receptors) are reported to be formed following prolonged agonist treatment of cells or whole animals. mu* receptors signal in the absence of activating ligand and a blockade of mu* activation of G-proteins by naloxone and naltrexone has been suggested to underlie the profound withdrawal syndrome precipitated by these antagonists in vivo. In this issue of the Journal, Divin et al. examined whether treatment of C6 glioma cells with mu-opioid receptor agonists produced constitutively active mu-opioid receptors or other commonly reported adaptations to prolonged agonist treatment. Adenylyl cyclase superactivation was readily apparent following agonist treatment but there was no evidence of the formation of constitutively active mu-opioid receptors. This result challenges the notion that prolonged agonist exposure inevitably produces mu* receptors, and is consistent with many studies of adaptations in neurons produced by chronic agonist treatment. The investigators provide no explanation of their failure to see mu* receptors in C6 cells, but this is perhaps understandable because the molecular nature of mu* receptors remains elusive, and the precise mechanisms that lead to their formation are unknown. Without knowing exactly what mu* receptors are, how they are formed and how they signal, understanding their role in cellular adaptations to prolonged opioid treatment will remain impossible. Studies such as this should refocus attention on establishing the molecular mechanisms that underlie that phenomenon of mu* receptors.

摘要

据报道,在对细胞或整个动物进行长时间激动剂处理后会形成组成型活性μ-阿片受体(μ受体)。μ受体在没有激活配体的情况下发出信号,并且有人提出纳洛酮和纳曲酮对μ激活G蛋白的阻断作用是这些拮抗剂在体内引发严重戒断综合征的基础。在本期《杂志》中,迪文等人研究了用μ-阿片受体激动剂处理C6胶质瘤细胞是否会产生组成型活性μ-阿片受体或其他通常报道的对长时间激动剂处理的适应性变化。激动剂处理后腺苷酸环化酶超活化很明显,但没有证据表明形成了组成型活性μ-阿片受体。这一结果挑战了长时间激动剂暴露必然会产生μ受体的观点,并且与许多关于慢性激动剂处理对神经元产生适应性变化的研究结果一致。研究人员没有解释他们在C6细胞中未能看到μ受体的原因,但这或许可以理解,因为μ受体的分子性质仍然难以捉摸,导致其形成的精确机制也不清楚。在不清楚μ受体究竟是什么、它们如何形成以及如何发出信号的情况下,理解它们在细胞对长时间阿片类药物处理的适应性变化中的作用将仍然是不可能的。这样的研究应该将注意力重新集中在确定μ受体现象背后的分子机制上。