Volume 16 Supplement 1

Abstracts from the 7th International Conference on cGMP Generators, Effectors and Therapeutic Implications

Open Access

Functions of NO-GC1 and NO-GC2 in pain processing

  • Jonas Petersen1Email author,
  • Evanthia Mergia2,
  • Oliver Drees1,
  • Ruirui Lu1,
  • Catherine Real1,
  • Andreas Friebe3,
  • Doris Koesling2 and
  • Achim Schmidtko1
BMC Pharmacology and Toxicology201516(Suppl 1):A74

DOI: 10.1186/2050-6511-16-S1-A74

Published: 2 September 2015

Background

Chronic pain in response to tissue inflammation (inflammatory pain) or nerve injury (neuropathic pain) is often unresponsive to currently available treatments. A large body of evidence indicates that production of nitric oxide (NO) and activation of NO-sensitive guanylyl cyclase (NO-GC) essentially contributes to the processing of chronic pain. NO-GC is a heterodimer consisting of one α subunit (α1 or α2) and one β1 subunit and exists in two isoforms (NO-GC1 and NO-GC2). However, the functional role of NO-GC1 and NO-GC2 in pain processing remains poorly understood. Here, we investigated the expression of NO-GC isoforms in pain-relevant tissues (dorsal root ganglia and the spinal cord) and characterized the nociceptive behavior of mice lacking α1 or α2 in models of acute nociceptive, inflammatory and neuropathic pain.

Conclusion

Our behavioral data point to different and partly contrary functions of NO-GC1 and NO-GC2 in the processing of inflammatory and neuropathic pain. The expression of NO-GC isoforms in dorsal root ganglia and the spinal cord is restricted to specific neuronal and non-neuronal cell populations. It remains to be determined which targets mediate the pain-relevant effects of NO-GC1 and NO-GC2.

Authors’ Affiliations

(1)
Institut für Pharmakologie und Toxikologie, Universität Witten/Herdecke
(2)
Institut für Pharmakologie und Toxikologie, Ruhr-Universität
(3)
Physiologisches Institut, Universität Würzburg

Copyright

© Petersen et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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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