Signal transduction mechanisms in primary afferent neurons following pain transmission

有令人信服的证据表明，不仅损伤的初级事件，而且其未损伤的相邻事件也表现出兴奋性和基因表达的改变，这些改变在伤害感觉、炎症反应和神经性疼痛中具有功能作用。我们研究了正常组织受到有害刺激或使用炎性疼痛模型或神经性疼痛模型后，初级传入神经元和脊髓神经元中几种形式的丝裂原活化蛋白激酶（MAPKs）动力学。在哺乳动物中，已经发现了四种主要的MAPK通路。它们是细胞外信号调节蛋白激酶1/2 （ERK1/2）、p38 MAPK、c-Jun n末端激酶（JNK）和ERK5。我们研究了MAPK在疼痛机制中的各种动态阶段，并发表了36篇被科学期刊接受的论文。

There is compelling evidence indicating that not only injured primary afferents, but also their spared neighbors, show an alteration of excitability and gene expression and that these changes have functional roles in nociception, inflammatory pan and neuropathic pain. We examined several forms of mitogen-activated protein kinases (MAPKs) dynamics in primary afferent neurons and also in spinal cord neurons following noxious stimuli to normal tissue or using inflammatory pain model or neuropathic pain model. In mammals, four major MAPK pathways have been discovered. They are the extracellular signal-regulated protein kinases 1/2 (ERK1/2), p38 MAPK, c-Jun N-terminal kinase (JNK), and ERK5. We examined a variety of phases of dynamics of MAPK in pain mechanisms and published 36 papers accepted in scientific journals.