Drake Robert A R, Hulse Richard P, Lumb Bridget M, Donaldson Lucy F
School of Physiology and Pharmacology, University of Bristol, Bristol, UK.
Cancer Biology, School of Medicine, University of Nottingham, Nottingham, UK.
J Physiol. 2014 Aug 15;592(16):3611-24. doi: 10.1113/jphysiol.2013.266494. Epub 2014 May 30.
Descending controls of spinal nociceptive processing play a critical role in the development of inflammatory hyperalgesia. Acute peripheral nociceptor sensitization drives spinal sensitization and activates spino-supraspinal-spinal loops leading to descending inhibitory and facilitatory controls of spinal neuronal activity that further modify the extent and degree of the pain state. The afferent inputs from hairy and glabrous skin are distinct with respect to both the profile of primary afferent classes and the degree of their peripheral sensitization. It is not known whether these differences in afferent input differentially engage descending control systems to different extents or in different ways. Injection of complete Freund's adjuvant resulted in inflammation and swelling of hairy hind foot skin in rats, a transient thermal hyperalgesia lasting <2 h, and longlasting primary mechanical hyperalgesia (≥7 days). Much longer lasting thermal hyperalgesia was apparent in glabrous skin (1 h to >72 h). In hairy skin, transient hyperalgesia was associated with sensitization of withdrawal reflexes to thermal activation of either A- or C-nociceptors. The transience of the hyperalgesia was attributable to a rapidly engaged descending inhibitory noradrenergic mechanism, which affected withdrawal responses to both A- and C-nociceptor activation and this could be reversed by intrathecal administration of yohimbine (α-2-adrenoceptor antagonist). In glabrous skin, yohimbine had no effect on an equivalent thermal inflammatory hyperalgesia. We conclude that acute inflammation and peripheral nociceptor sensitization in hind foot hairy skin, but not glabrous skin, rapidly activates a descending inhibitory noradrenergic system. This may result from differences in the engagement of descending control systems following sensitization of different primary afferent classes that innervate glabrous and hairy skin.
脊髓伤害性信息处理的下行控制在炎症性痛觉过敏的发展中起关键作用。急性外周伤害感受器敏化驱动脊髓敏化,并激活脊髓-脊髓上-脊髓环路,导致对脊髓神经元活动的下行抑制和易化控制,进而进一步改变疼痛状态的程度和强度。来自有毛皮肤和无毛皮肤的传入输入在初级传入神经类别概况及其外周敏化程度方面均有所不同。尚不清楚这些传入输入的差异是否会以不同程度或不同方式使下行控制系统产生不同的参与。注射完全弗氏佐剂会导致大鼠后足有毛皮肤发生炎症和肿胀、持续时间小于2小时的短暂性热痛觉过敏,以及持续时间较长的原发性机械性痛觉过敏(≥7天)。在无毛皮肤中,明显出现持续时间长得多的热痛觉过敏(1小时至超过72小时)。在有毛皮肤中,短暂性痛觉过敏与对A类或C类伤害感受器热激活的退缩反射敏化有关。痛觉过敏的短暂性归因于一种迅速启动的下行抑制性去甲肾上腺素能机制,该机制影响对A类和C类伤害感受器激活的退缩反应,并且鞘内注射育亨宾(α-2肾上腺素能受体拮抗剂)可使其逆转。在无毛皮肤中,育亨宾对同等程度的热炎症性痛觉过敏没有影响。我们得出结论,后足有毛皮肤而非无毛皮肤中的急性炎症和外周伤害感受器敏化会迅速激活下行抑制性去甲肾上腺素能系统。这可能是由于支配无毛皮肤和有毛皮肤的不同初级传入神经类别敏化后下行控制系统参与情况的差异所致。