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. 2018 Feb 9;14:1744806918761238. doi: 10.1177/1744806918761238

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© The Author(s) 2018

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) 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 pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Intrathecal (i.t.) pre-treatment with BmK AGAP inhibited CCI-induced neuropathic pain. (a) Schematic illustration of pre-treatment experimental protocol. (b) Pre-treatment with BmK AGAP (5 µg) prevented CCI-induced thermal hyperalgesia in the PWL test and (c) mechanical allodynia in the PWT test. *P < 0.05, **P < 0.01, compared with Sal + Sham group; ^#P < 0.05, ^##P < 0.01, compared with Sal + CCI group, n = 8 mice in each group. CCI: chronic constrictive injury; PWL: paw-withdrawal latency; PWT: paw-withdrawal threshold.