吗啡在体外可直接刺激痛觉感受器。

IF 2.8 3区 医学 Q2 NEUROSCIENCES
Eugen V Khomula, Jon D Levine
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引用次数: 0

摘要

超痛诱导是一种从急性疼痛向慢性疼痛过渡的临床前模型,其特点是前列腺素 E2(PGE2)诱导的机械超痛的剂量-反应曲线左移并明显延长。在体外,前列腺素 E2 诱导的痛觉感受器敏化的浓度依赖性向左移动,这就是痛觉感受器启动的特征。在本体外研究中,我们测试了缪阿片受体(MOR)激动剂阿片类镇痛药吗啡通过直接作用于痛觉感受器而产生引诱作用的假设。我们报告说,在体外用吗啡处理痛觉感受器时,PGE2 诱导的痛觉感受器敏化的浓度依赖性会向左移动。我们的研究结果支持了阿片类药物直接作用于痛觉感受器诱导引物的观点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Morphine acts in vitro to directly prime nociceptors.

Hyperalgesic priming is a preclinical model of the transition from acute to chronic pain characterized by a leftward shift in the dose-response curve for and marked prolongation of prostaglandin E2 (PGE2)-induced mechanical hyperalgesia, in vivo. In vitro, priming in nociceptors is characterized by a leftward shift in the concentration dependence for PGE2-induced nociceptor sensitization. In the present in vitro study we tested the hypothesis that a mu-opioid receptor (MOR) agonist opioid analgesic, morphine, can produce priming by its direct action on nociceptors. We report that treatment of nociceptors with morphine, in vitro, produces a leftward shift in the concentration dependence for PGE2-induced nociceptor sensitization. Our findings support the suggestion that opioids act directly on nociceptors to induce priming.

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来源期刊
Molecular Pain
Molecular Pain 医学-神经科学
CiteScore
5.60
自引率
3.00%
发文量
56
审稿时长
6-12 weeks
期刊介绍: Molecular Pain is a peer-reviewed, open access journal that considers manuscripts in pain research at the cellular, subcellular and molecular levels. Molecular Pain provides a forum for molecular pain scientists to communicate their research findings in a targeted manner to others in this important and growing field.
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