Secondary hyperalgesia and presynaptic inhibition:: an update
Secondary hyperalgesia and presynaptic inhibition:: an update
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DOI：
10.1016/s1090-3801(03)00047-8
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发表时间：
2003-01-01
影响因子：
3.6
通讯作者：
García-Nicas, E
中科院分区：
文献类型：
--
作者：
Cervero, F;Laird, JMA;García-Nicas, E
继发性痛觉过敏最突出的特征之一是触摸诱发的疼痛，即，由施加到邻近或远离原始损伤的区域的动态触觉刺激引起的疼痛。一般认为，这种感觉改变的神经生物学机制涉及中枢神经系统（CNS），因此来自继发性痛觉过敏区域的低阈值机械感受器中的传入脉冲可以引起疼痛感觉而不是触摸。几年前，我们提出了一个机制模型，这种形式的疼痛的基础上突触前的相互作用，在脊髓背角之间的终端的低阈值机械感受器和伤害性感受器。在这里，我们回顾了收集的证据，在此期间的几年中，特别提到的逆向活动（背根反射-DRR）在伤害性传入和收购的低阈值输入的伤害性感受器特异性神经元在脊髓背角的实验研究支持这个模型。我们还讨论和确定潜在的分子机制，可能是突触前相互作用模型的基础，因此可能是继发性痛觉过敏的发展负责。(C)2003年，国际疼痛研究协会欧洲分会联合会。由Elsevier Science Ltd.出版，版权所有。
One of the most prominent features of secondary hyperalgesia is touch-evoked pain, i.e., pain evoked by dynamic tactile stimuli applied to areas adjacent or remote from the originating injury. It is generally accepted that the neurobiological mechanism of this sensory alteration involves the central nervous system (CNS) so that incoming impulses in low-threshold mechanoreceptors from the area of secondary hyperalgesia can evoke painful sensations instead of touch. Some years ago we proposed a mechanistic model for this form of pain based on presynaptic interactions in the spinal dorsal horn between the terminals of low-threshold mechanoreceptors and of nociceptors. Here we review the evidence gathered in support of this model in the intervening years with special reference to experimental studies of antidromic activity (Dorsal Root Reflexes - DRRs) in nociceptive afferents and on the acquisition of low-threshold inputs by nociceptor-specific neurons in the spinal dorsal horn. We also discuss and identify potential molecular mechanisms that may underlie the presynaptic interaction model and therefore that could be responsible for the development of secondary hyperalgesia. (C) 2003 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Science Ltd. All rights reserved.