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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.

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。

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