Sato J, Perl E R
University of North Carolina, Department of Physiology, Chapel Hill 27599.
Science. 1991 Mar 29;251(5001):1608-10. doi: 10.1126/science.2011742.
The mechanisms by which peripheral nerve injuries sometimes lead to causalgia, aberrant burning pain peripheral to the site of nerve damage, are uncertain, although the sympathetic nervous system is known to be involved. Whether such syndromes could be the result of the development of responsiveness by some cutaneous pain receptors (C-fiber nociceptors) to sympathetic efferent activity as a consequence of the nerve injury was tested in an animal model. After nerve damage but not in its absence, sympathetic stimulation and norepinephrine were excitatory for a subset of skin C-fiber nociceptors and enhanced the responsiveness of these nociceptors to tissue-damaging stimulation. These effects were demonstratable within days after nerve lesions, occurred at the cutaneous receptive terminal region, were manifest in sensory fibers that had not degenerated after the injury, and were mediated by alpha 2-adrenergic-like receptors.
周围神经损伤有时会导致灼性神经痛，即神经损伤部位周围出现异常灼痛，其机制尚不清楚，尽管已知交感神经系统与之有关。在一个动物模型中，研究了此类综合征是否可能是由于神经损伤导致一些皮肤痛觉感受器（C纤维伤害感受器）对交感传出活动产生反应性的结果。神经损伤后而非未损伤时，交感神经刺激和去甲肾上腺素对一部分皮肤C纤维伤害感受器具有兴奋性，并增强了这些伤害感受器对组织损伤性刺激的反应性。这些效应在神经损伤后的数天内即可显现，发生于皮肤感受终端区域，在损伤后未发生退变的感觉纤维中表现明显，且由α2 -肾上腺素能样受体介导。
