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. 2015 Nov 5;11:68. doi: 10.1186/s12990-015-0073-7

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© Chen et al. 2015

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. 5 — p38 is downstream of P2X7R-P2Y1R control of P2X3R expression. a Blocking P2X7R activation with the P2X7R antagonist, A740003 (A74) (250 nM), caused an increase in the P2X3R expression in DRGs [A74/Con, 2.17 ± 0.13, n(Con) = 14, n (A74) = 9]. Activating p38 with Anis (10 nM) overrode the enhancing effect of A74 on P2X3R expression [(Anis + A74)/Con = 0.98 ± 0.11, n(Con) = 14, n (Anis + A74003) = 9]. b Blocking P2Y1R activation with MRS increased P2X3R expression [MRS/Con, 2.17 ± 0.19, n(Con) = 14, n(MRS) = 9]. In the presence of Anis, MRS no longer augmented the P2X3R expression [(Anis + MRS)/Con = 0.93 ± 0.14, n(Con) = 14, n(Anis + MRS) = 8]. NS: P > 0.05; *P < 0.05 compared with [A74 (−) + Anis (−)] (a) or with [MRS (−) + Anis (−)] (b); ^#P < 0.05 compared with [A74 (+) + Anis (+)] (a) or with [MRS (+) + Anis (+)] (b)