کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4325564 | 1614012 | 2012 | 13 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Activation of satellite glial cells in lumbar dorsal root ganglia contributes to neuropathic pain after spinal nerve ligation Activation of satellite glial cells in lumbar dorsal root ganglia contributes to neuropathic pain after spinal nerve ligation](/preview/png/4325564.png)
The 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 4 h 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 7 d 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.
► SGCs in DRG were activated after L5 spinal nerve ligation.
► The application of fluorocitrate into L5 DRG significantly alleviated mechanical allodynia.
► SGC activation contributed to the early maintenance of allodynia after SNL.
► Targeting SGCs may open a range of new possibilities for curing neuropathic pain.
Journal: Brain Research - Volume 1427, 3 January 2012, Pages 65–77