• Feng-Yu Liu, Yan-Ni Sun, Fa-Tian Wang, Qian Li, Li Su, Zi-Fang Zhao, Xiang-Ling Meng, Hong Zhao, Xi Wu, Qian Sun, Guo-Gang Xing, and You Wan.
• Neuroscience Research Institute, Peking University, Beijing 100191, PR China.
• Brain Res. 2012 Jan 3;1427:65-77.

AbstractThe role of satellite glial cells (SGCs) of sensory ganglia in chronic pain begins to receive interest. The present study aims to investigate the contribution of SGC activation to the development of neuropathic pain. A neuropathic pain model was established by lumbar 5 spinal nerve ligation (SNL), and glial fibrillary acidic protein (GFAP) was used as a marker of SGC activation. It was found that SGCs were activated in the ipsilateral dorsal root ganglia (DRG) increased significantly as early as 4h following SNL, gradually increased to a peak level at day 7, and then stayed at a high level to the end of the experiment at day 56. SGC activation in the SNL group was significantly higher than that in the sham group at days 1, 3 and 7 after operation. Immunofluorescent double labeling showed that the activated SGCs encircled large, medium-sized and small neurons. The SGCs surrounded the small and medium-sized neurons were preferentially activated in the early phase, but shifted to large diameter neurons as time went on. Continuous infusion of fluorocitrate, a glial metabolism inhibitor, to the affected DRG via mini-osmotic pump for 7d significantly alleviated mechanical allodynia at day 7. These results suggest that SGCs in the DRG were activated after SNL. SGC activation contributed to the early maintenance of neuropathic pain.Copyright © 2011 Elsevier B.V. All rights reserved.

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