Pain: Molecular mechanisms
Pain: Molecular mechanisms
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DOI：
10.1054/jpai.2000.9818
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发表时间：
2000-09-01
期刊：
影响因子：
4
通讯作者：
Woolf, CJ
中科院分区：
文献类型：
--
作者：
Costigan, M;Woolf, CJ
近年来，我们在分子和细胞水平上对慢性炎症性和神经性疼痛的理解以惊人的速度发展。炎症性或神经病性神经元可塑性描述了参与疼痛传递的神经元从正常敏感性状态转变为超敏感性状态的过程。在这里，我们总结了目前的理论，在分子背景下，体感神经可塑性，突出关键受体，离子通道，和信号分子参与。我们还提出了药物设计的新的可能性，基于这些分子球员的合理靶向。
Our understanding of chronic inflammatory and neuropathic pain at the molecular and cellular level has developed at an extraordinary rate in recent years. Inflammatory, or neuropathic, neuronal plasticity describes the process by which the neurons involved in pain transmission are converted from a state of normosensitivity to one in which they are hypersensitive. Here we summarize current theories on somatosensory neuroplasticity in a molecular context, highlighting key receptors, ion channels, and signal molecules involved. We also suggest new possibilities for drug design, based on the rational targeting of these molecular players.