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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 8. — Adenosine signaling modulates pain hypersensitivity behaviors in resiniferatoxin (RTX) neuropathy. This diagram shows an analgesia pathway in small-fiber neuropathy: (left panel) membrane-bound PAP hydrolysis AMP into adenosine (1) which activates A1Rs as the cellular analgesia mechanism (2). (3) TRPV1 coexpressed with PAP and A1Rs, and TRPV1 were depleted by RTX, causes a decrease in analgesic adenosine signaling, including a reduction in PAP ectonucleotidase activity and A1Rs depletion (dotted profiles in right panel). The reduced PAP ectonucleotidase activity causes a decrease in extracellular AMP hydrolysis (4), which results in a reduction in adenosine. (5) A parallel reduction of A1R(+) leads to the disability of adenosine signaling and further exacerbates the development of pain hypersensitivity (6). A1R, adenosine A1 receptor; AMP, adenosine monophosphate; PAP, prostatic acid phosphatase; TRPV1, transient receptor potential vanilloid type 1.