OPIOIDS SUPPRESS SPONTANEOUS ACTIVITY OF POLYMODAL NOCICEPTORS IN RAT PAW SKIN INDUCED BY ULTRAVIOLET-IRRADIATION
OPIOIDS SUPPRESS SPONTANEOUS ACTIVITY OF POLYMODAL NOCICEPTORS IN RAT PAW SKIN INDUCED BY ULTRAVIOLET-IRRADIATION
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DOI：
10.1016/0306-4522(94)90456-1
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发表时间：
1994-02-01
期刊：
影响因子：
3.3
通讯作者：
DRAY, A
中科院分区：
文献类型：
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作者：
ANDREEV, N;URBAN, L;DRAY, A
在成年大鼠隐神经-后爪皮肤的体外制备中，研究了损伤或炎症后周围伤害感受器的化学敏感性的变化。通过预先紫外线照射诱导后爪中的热痛觉过敏，并在5天后研究这些动物的皮肤。多模态伤害性感受器在正常皮肤中是静止的，但在紫外线照射后在大多数纤维中是自发活动的。紫外线预处理后，辣椒素诱导的细纤维活化增强。直接给药吗啡，DAGOL（μ受体激动剂）和U-69593（κ受体激动剂），但不DPDPE（δ受体激动剂）的感受野产生浓度相关的和纳洛酮可逆的抑制自发放电的多模态伤害感受器的紫外线处理的皮肤。吗啡并没有减少正常皮肤中的纤维的活动时，这些都是由KCl depolarization.These数据表明，多模态伤害感受器改变其活性和敏感性外源性化学物质的诱导外周痛觉过敏的紫外线照射。具体地说，提供了通过μ-和κ-阿片受体表达阿片样物质敏感性和抑制多模态伤害感受器活性的证据。这些观察结果可以解释阿片类药物在外周痛觉过敏的特定状态下的外周抗伤害性作用。
Changes in chemical sensitivity of periperal nociceptors following injury or inflammation have been studied in in vitro preparation of the saphenous nerve-hind paw skin from adult rats. Heat hyperalgesia in the hind paw was induced by a prior ultraviolet irradiation and the skin from these animals was investigated five days later. Polymodal nociceptors were quiescent in normal skin but were spontaneously active in the majority of fibres after ultraviolet exposure. Capsaicin-induced activation of fine fibres was enhanced after ultraviolet pretreatment. Direct administration of morphine, DAGOL (mu-receptor agonist) and U-69593 (kappa-receptor agonist), but not DPDPE (delta-receptor agonist) to the receptive field produced a concentration related and naloxone-reversible suppression of spontaneous firing in polymodal nociceptors of ultraviolet-treated skin. Morphine did not reduce the activity of fibres in normal skin when these were driven by KCl depolarization.These data show that polymodal nociceptors change their activity and sensitivity to exogenous chemicals following the induction of peripheral hyperalgesia by ultraviolet irradiation. Specifically, evidence is provided for the expression of opioid sensitivity and inhibition of polymodal nociceptor activity through mu- and kappa-opioid receptors. These observations may account for peripheral antinociceptive actions of opioids during specific states of peripheral hyperalgesia.