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Activation of glia and microglial p38 MAPK in medullary dorsal horn contributes to tactile hypersensitivity following trigeminal sensory nerve injury

Cited 168 time in Web of Science Cited 174 time in Scopus
Authors
Piao, Zheng Gen; Cho, Ik-Hyun; Park, Chul Kyu; Hong, Jin Pyo; Choi, Se-Young; Lee, Sung Joong; Lee, Seungbok; Park, Kyungpyo; Kim, Joong Soo; Oh, Seog Bae
Issue Date
2006-04
Publisher
Elsevier
Citation
Pain. 2006;121(3):219-231
Keywords
c-FosGFAPGliaInferior alveolar nerveMedullary dorsal hornMental nerveMinocyclineOX-42p38 mitogen-activated protein kinaseTactile hypersensitivity
Abstract
Glial activation is known to contribute to pain hypersensitivity following spinal sensory nerve injury. In this study, we investigated mechanisms by which glial cell activation in medullary dorsal horn (MDH) would contribute to tactile hypersensitivity following inferior alveolar nerve and mental nerve transection (IAMNT). Activation of microglia and astrocytes was monitored at 2 h, 1, 3, 7, 14, 28, and 60 days using immunohistochemical analysis with OX-42 and GFAP antibodies, respectively. Tactile hypersensitivity was significantly increased at 1 day, and this lasted for 28 days after IAMNT. Microglial activation, primarily observed in the superficial laminae of MDH, was initiated at 1 day, maximal at 3 days, and maintained until 14 days after IAMNT. Astrocytic activation was delayed compared to that of microglia, being more profound at 7 and 14 days than at 3 days after IAMNT. Both tactile hypersensitivity and glial activation appeared to gradually reduce and then return to the basal level by 60 days after IAMNT. There was no significant loss of trigeminal ganglion neurons by 28 days following IAMNT, suggesting that degenerative changes in central terminals of primary afferents might not contribute to glial activation. Minocycline, an inhibitor of microglial activation, reduced microglial activation, inhibited p38 mitogen-activated protein kinase (MAPK) activation in microglia, and significantly attenuated the development of pain hypersensitivity in this model. These results suggest that glial activation in MDH plays an important role in the development of neuropathic pain and activation of p38 MAPK in hyperactive microglia contributes to pain hypersensitivity in IAMNT model.
ISSN
0304-3959
Language
English
URI
http://hdl.handle.net/10371/69745
DOI
https://doi.org/10.1016/j.pain.2005.12.023
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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