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. 2017 Sep 12;14:185. doi: 10.1186/s12974-017-0960-0

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Intrathecal injection of AM1241 attenuated CCI-induced hyperalgesia. Pain sensitivity was determined by measuring TWL on the day before CCI and on days 1, 3, 5, 7, 10, and 14 after nerve injury. After nerve injury, the TWL in the vehicle-treated CCI group (0.005% DMSO) was significantly lower than that in the sham group (*P < 0.05). No significant difference was identified between the vehicle-treated CCI group and 1pM AM1241-treated CCI group. At 1, 3, 5, 7, 10, and 14 days after nerve injury, the TWL in the 10- and 100pM AM1241-treated CCI rats were significantly higher than that in the vehicle-treated CCI group (10pM: ⁺ P < 0.05; 100pM: ⁺ P < 0.05). All values represent mean ± standard deviation (n = 8). *P < 0.05 compared with the sham group; ⁺ P < 0.05 compared with the vehicle-treated CCI group