Analysis of therapeutic mechanisms of Bushi by using in vivo imaging

本研究的目的是阐明躯体感觉皮层(S1)的神经胶质功能在神经病理性疼痛发病机制中的作用。使用活体双光子显微镜，我研究了对照组和神经病理性疼痛模型动物(SNL；脊神经结扎)的S1皮质星形胶质细胞内钙活性的时间进程，并平行于疼痛行为(痛觉异常)。我发现(1)SNL增强了S1皮层的钙活性，(2)S1星形胶质细胞的X受体被重新唤醒，(3)神经病理性疼痛依赖于(1)和(2)。这些数据强烈提示，S1星形胶质细胞内钙离子活性异常，以及随后发生的事件可能参与了神经病理性疼痛的发生或发展。

The aim of this study is to clarify an involvement of glial functions in the somatosensory cortex (S1) in the pathogenesis of neuropathic pain. Using in vivo 2 photon microscopy, I investigated chronologic time-courses of Ca2+ activities in S1 cortical astrocytes both in control and neuropathic pain model animals (SNL; spinal nerve ligation), in parallel with pain behaviors (allodynia). I found that (1) Ca2+ activities in S1 cortex was enhanced by SNL, (2) receptor X was re-awaken in S1 astrocytes, and (3) neuropathic pain was dependent on both (1) and (2). These data strongly suggest that abnormal Ca2+ activities in S1 astrocytes, and subsequent events should be involved in the cause or the development of neuropathic pain.