Research for the mechanism of the expression of neuropathic pain

我们已经报道，激活的小胶质细胞在神经损伤后通过刺激P2X4受体而引起对吗啡具有抵抗力的神经病理性疼痛具有主要作用(Nature，2003&2005)。在本研究中，我们试图找出小胶质细胞是如何接受神经损伤信息并导致疼痛的。小胶质细胞是通过损伤神经释放的细胞因子如CCL21、干扰素-γ、血小板衍生生长因子等激活的。此外，转录因子STAT3仅在神经损伤后的星形胶质细胞中被激活，这在诱发神经病理性疼痛中起着非常重要的作用。

We had already reported that activated microglia have a main role for evoking neuropathic pain which is resistant to morphine through the stimulation of P2X4 receptors after nerve damages (Nature, 2003 & 2005). In the present study, we tried to find how microglia receive information of nerve damage and cause the pain. It was clarified that microglia are activated through cytokines such as CCL21 released from the damage nerve, interferon-γ, PDGF. Moreover, transcription factor STAT3 was activated only in astrocytes after nerve damage that is very important for the evoking neuropathic pain.