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. 2016 May 12;12:1744806916646784. doi: 10.1177/1744806916646784

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© The Author(s) 2016

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 5. — Genetic deletion of IL-1R1 prevents both abnormal behaviors and the overexpression of IL-1β induced by SNI in mice. (a–d) Paw withdrawal threshold, recognition index for STM, and floating time in wild type (WT) mice with or without SNI and IL-1R1 knockout (KO) mice with SNI or without SNI are shown (n = 7–12/group). (e) The Western blots show the expression of IL-1β in SDH, hippocampus, PFC, NAcc, and AMG in the different groups as indicated (n = 5–6 in each group). *P < .05; **P < .01; ***P < .001 vs. WT naïve mice; ^#P < .05; ^##P < .01; ^###P < .001 vs. WT + SNI mice. SNI: spared nerve injury; SDH: spinal dorsal horn; NAcc: nucleus accumbens; AMG: amygdala.