Ultraviolet-B-induced mechanical hyperalgesia: A role for peripheral sensitisation
Ultraviolet-B-induced mechanical hyperalgesia: A role for peripheral sensitisation
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DOI：
10.1016/j.pain.2010.04.018
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发表时间：
2010-07-01
期刊：
影响因子：
7.4
通讯作者：
McMahon, Stephen B.
中科院分区：
文献类型：
--
作者：
Bishop, Thomas;Marchand, Fabien;McMahon, Stephen B.
紫外线（UV）诱导的皮肤炎症正在成为一种具有新颖感觉表型的疼痛模型。1000兆焦耳/厘米(2)的中波紫外线剂量会产生高度显著的热和机械超敏反应。在这里，我们研究了大鼠这种痛觉过敏的性质和机制。值得注意的是，机械性痛觉过敏（戒断阈值变化接近60%）仅限于病变部位，邻近未辐照皮肤的机械阈值没有变化（即无继发性超敏反应），提示其周围机制。与此一致的是，我们发现在鞘内使用10 μ g的nmda受体拮抗剂MK-801后，原发性机械超敏反应没有明显变化。使用体外皮肤神经制剂，在存在和不存在uvb炎症的情况下，记录了103种外周伤害感受器对6-768 μ m皮肤位移刺激的阈上反应。在uvb诱导的痛觉过敏的高峰期，我们观察到从uvb发炎的皮肤（n = 19）记录的ad -伤害感受器的机械反应特性与从原始皮肤（n = 13）记录的相比显着降低了50%。与未接触皮肤（n = 12）相比，uvb发炎皮肤（n = 26）的热敏c -伤害感受器的机械反应特性没有变化，但它们的热反应显著增加，增幅接近75%。然而，与未接触皮肤（n = 12）相比，热不敏感的c -伤害感受器在uvb炎症（n = 21）中对机械刺激的反应特性显着增强（约60%）。值得注意的是，ad和热不敏感的c -伤害感受器的机械反应的改变是对强刺激的特殊改变。该剂量的UVB未诱导自发活性。我们的结论是，uvb诱导的机械性痛觉过敏可以通过外周伤害感受器反应特性的净转移来解释。(C) 2010国际疼痛研究协会。Elsevier b.v.版权所有。
Ultraviolet (UV) induced cutaneous inflammation is emerging as a model of pain with a novel sensory phenotype. A UVB dose of 1000 mJ/cm(2) produces a highly significant thermal and mechanical hypersensitivity. Here we examined the properties and mechanisms of such hyperalgesia in rats. Significantly, the mechanical hyperalgesia (with similar to 60% change in withdrawal thresholds) was restricted to the lesion site with no changes in mechanical threshold in adjacent non-irradiated skin (i.e. no secondary hypersensitivity), suggesting a peripheral mechanism. Consistent with this, we found that primary mechanical hypersensitivity showed no significant changes after intrathecal treatment with 10 mu g of the NMDA-receptor antagonist MK-801. Using an in vitro skin-nerve preparation, in the presence and absence of UVB-inflammation, suprathreshold responses to skin displacement stimuli of 6-768 mu m of 103 peripheral nociceptors were recorded. At the peak of UVB-induced hyperalgesia we observed that mechanical response properties of Ad-nociceptors recorded from UVB-inflamed skin (n = 19) were significantly diminished, by similar to 50%, compared to those recorded from naive skin (n = 13). The mechanical response properties of heat-sensitive C-nociceptors were unchanged while their heat responses were significantly increased, by similar to 75%, in UVB-inflamed (n = 26) compared to naive skin (n = 12). Heat-insensitive C-nociceptors, however, demonstrated significantly enhanced (by similar to 60%) response properties to mechanical stimulation in UVB-inflamed (n = 21) compared to naive skin (n = 12). Notably alteration in mechanical responses of Ad-and heat-insensitive C-nociceptors were particular to stronger stimuli. Spontaneous activity was not induced by this dose of UVB. We conclude that UVB-induced mechanical hyperalgesia may be explained by a net shift in peripheral nociceptor response properties. (C) 2010 International Association for the Study of Pain. Published by Elsevier B. V. All rights reserved.