痛觉过敏启动是从急性到慢性疼痛过渡的临床前模型，其特征是前列腺素E2（PGE2）诱导的机械性痛觉过敏的剂量反应曲线向左移动并明显延长，在体内。体外，伤害感受器的启动特征是PGE2诱导的伤害感受器致敏的浓度依赖性向左移动。在目前的体外研究中，我们测试了mu-阿片受体（MOR）激动剂阿片类镇痛药的假设，吗啡,可以通过对伤害感受器的直接作用产生启动作用。我们报道用吗啡治疗伤害性感受器，在体外，对PGE2诱导的伤害感受器致敏的浓度依赖性产生向左移动。我们的发现支持阿片类药物直接作用于伤害感受器以诱导引发的建议。
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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