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. 2017 Jun 21;7:4005. doi: 10.1038/s41598-017-04198-3

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Spinal CXCR4-PLC-CaMKII pathway is involved in SDF-1-induced pain hypersensitivity. Intrathecal injection of exogenous SDF-1 (5 μg/10 μl) markedly induced mechanical allodynia (A,C and E) and thermal hyperalgesia (B,D and F) in a time-dependent manner. Post-administration of CXCR4 inhibitor Plerixafor (10 μg/10 μl, A and B), PLC inhibitor U73122 (10 nM/10 μl, C and D) or CaMKII inhibitor AIP2 (10 μM/10 μl, E and F), 30 min after SDF-1 injection, partially reversed SDF-1-induced nociceptive behaviors. The behavioral experiments between groups were performed at the same time points under the same experimental conditions. The same data of naive group and naive + SDF-1 group were rearranged and reused in A/C/E (threshold) and B/D/F (latency), respectively, to present the behavioral results more clearly and minimize the number of animals used. *P < 0.05, **P < 0.01 versus naive group; ^# P < 0.05, ^## P < 0.01 vs naive + SDF-1 group; n = 8 for each group.