Basic & Clinical Medicine ›› 2011, Vol. 31 ›› Issue (2): 222-224.

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Update in molecular mechanism of pain

MA Lu-lu 1,LIU Wei 2,HUANG Yu-guang 1   

  1. 1. PUMC Hospital, CAMS & PUMC
    2.
  • Received:2010-01-18 Revised:2010-05-26 Online:2011-02-05 Published:2011-03-14
  • Contact: HUANG Yu-guang E-mail:pumchhyg@yahoo.com.cn

Abstract: Neuropathic pain is a chronic condition affecting millions of people worldwide, and current treatments are often inadequate, ineffective or associated with potential severe side effects. A great deal of researches in the past decade have demonstrated the activation of glial constitutes a vital signaling network between pre-synaptic neurons and post-synaptic neurons, contributing to the release of cytokines、chemotaxin、proinflammatory factors and tumor necrosis factor, facilating the kinase pathways and finally leading to the activation of neurons. Clinical manifestations include hyperalgesia and allodynia. However further understanding of pain mechanism, especially molecular mechanism will help us find the new target therapy for pain.

Key words: pain,sodium channel,microglia,Extracellular signal-regulated MAP kinases

CLC Number: