Title |
Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons
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Published in |
Journal of Neuroinflammation, January 2014
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DOI | 10.1186/1742-2094-11-7 |
Pubmed ID | |
Authors |
Chung-Yu Huang, Ying-Ling Chen, Allen H Li, Juu-Chin Lu, Hung-Li Wang |
Abstract |
Several lines of evidence suggest that CCL2 could initiate the hyperalgesia of neuropathic pain by causing central sensitization of spinal dorsal horn neurons and facilitating nociceptive transmission in the spinal dorsal horn. The cellular and molecular mechanisms by which CCL2 enhances spinal pain transmission and causes hyperalgesia remain unknown. The substantia gelatinosa (lamina II) of the spinal dorsal horn plays a critical role in nociceptive transmission. An activated spinal microglia, which is believed to release pro-inflammatory cytokines including TNF-α, plays an important role in the development of neuropathic pain, and CCL2 is a key mediator for spinal microglia activation. In the present study, we tested the hypothesis that spinal CCL2 causes the central sensitization of substantia gelatinosa neurons and enhances spinal nociceptive transmission by activating the spinal microglia and augmenting glutamatergic transmission in lamina II neurons. |
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Demographic breakdown
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
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Spain | 1 | 3% |
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Unknown | 37 | 95% |
Demographic breakdown
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Student > Ph. D. Student | 10 | 26% |
Researcher | 6 | 15% |
Student > Bachelor | 6 | 15% |
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Professor > Associate Professor | 4 | 10% |
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