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. 2018 Jul 25;159(8):1580–1591. doi: 10.1097/j.pain.0000000000001246

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Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Figure 5. — Expression of adenosine A1 receptors (A1Rs) in resiniferatoxin (RTX) neuropathy. (A–F) Double-labeling immunofluorescence staining was performed on dorsal root ganglion (DRG) sections with anti-A1R (A, C, D, and F in green) and anti-transient receptor potential vanilloid subtype 1 (TRPV1; B, C, E, and F in red) antisera in the vehicle (A–C) and day 7 after RTX neuropathy (RTX group) (D–F). (C and F) The images show the colocalization of A1R and TRPV1 DRG neurons in the vehicle (C) and RTX (F) groups. Arrow indicated the colocalization of A1R and TRPV1 expression DRG neurons. (G) The graph shows the histogram of diameters for A1R(+) neurons in the vehicle group (n = 819 neurons). (H) The diagram indicates the ratios of A1R(+)/TRPV1(+) (open bar, n = 5) and TRPV1(+)/A1R(+) (filled bar, n = 5) in the vehicle group in (A–F). (I) The graph shows the density changes in A1R(+) neurons in the vehicle (open bar, n = 10) and RTX (filled bar, n = 7) groups. ***P < 0.001. Bar, 50 µm.