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. 2020 Aug 18;36(11):1344–1354. doi: 10.1007/s12264-020-00557-9

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — CCL2 enhances NMDA currents via GluN2B activation. A, B Western blots showing that CCL2 induces a significant increase in GluN2B expression. C, D Ifenprodil, a GluN2B blocker, partially inhibits NMDAR-induced currents in lamina IIo neurons and abolishes the CCL2-induced enhancement of these currents. E, F Behavioral tests showing that CFA-induced mechanical allodynia and thermal hyperalgesia are reversed by i.p. Ifenprodil. *P < 0.05, ⁺⁺P < 0.01, n = 6–8.