Chen X, Tanner K, Levine J D
Department of Anatomy, University of California, San Francisco 94143, USA.
Neurosci Lett. 1999 May 28;267(2):105-8. doi: 10.1016/s0304-3940(99)00345-6.
While it is generally assumed that nociceptor sensitization underlies peripheral hyperalgesia, there is disagreement regarding the ability of inflammatory mediators to sensitize nociceptors to mechanical stimuli. In this in vivo electrophysiological study, mechanical threshold and response to sustained threshold and sustained suprathreshold mechanical stimuli were measured before and after intradermal administration of prostaglandin E2 (PGE2) into the receptive field of cutaneous C-fiber nociceptors in the rat. PGE2 produced a decrease in mechanical threshold and an increase in response to sustained threshold but not sustained suprathreshold mechanical stimulation. These data suggest that while inflammatory mediators produce a decrease in mechanical threshold and/or an increase in number of action potentials to sustained threshold stimuli, they do not increase the maximal response to mechanical stimuli in C-fiber nociceptors.
虽然一般认为伤害感受器敏化是外周性痛觉过敏的基础，但关于炎症介质使伤害感受器对机械刺激敏感化的能力存在分歧。在这项体内电生理研究中，在大鼠皮肤C纤维伤害感受器的感受野内皮内注射前列腺素E2（PGE2）之前和之后，测量了机械阈值以及对持续阈值和持续超阈值机械刺激的反应。PGE2使机械阈值降低，对持续阈值刺激的反应增加，但对持续超阈值机械刺激的反应未增加。这些数据表明，虽然炎症介质会使机械阈值降低和/或对持续阈值刺激的动作电位数量增加，但它们不会增加C纤维伤害感受器对机械刺激的最大反应。
