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Research ArticleCellular and Molecular

Dual Regulation of δ-Opioid Receptor Function by Arachidonic Acid Metabolites in Rat Peripheral Sensory Neurons

Laura C. Sullivan, Kelly A. Berg and William P. Clarke
Journal of Pharmacology and Experimental Therapeutics April 2015, 353 (1) 44-51; DOI: https://doi.org/10.1124/jpet.114.221366
Laura C. Sullivan
Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Kelly A. Berg
Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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William P. Clarke
Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Abstract

The regulation of opioid receptor system function in peripheral sensory neurons is not well understood. Opioid agonist efficacy to inhibit nociceptor function and to promote antinociception is generally weak under basal conditions and frequently no response occurs. However, in response to a cyclooxygenase-dependent metabolite of arachidonic acid (AA) after exposure to inflammatory mediators, such as bradykinin (BK) or exogenous AA, peripheral opioid receptor systems become much more responsive to opioid agonists. In this study, we examined the time course for the induction and maintenance of functional competence of the δ-opioid receptor (DOR) system in adult rat nociceptors in culture and in vivo. We found that the responsive state of DOR after pretreatment with BK or exogenous AA is transient (30–60 minutes) and persists for 15–30 minutes after a 15-minute exposure of nociceptors to BK or AA. Interestingly, whereas functional competence of the DOR system could be reinduced with a second application of BK 60 minutes after the first, responsiveness of the DOR system could not be reinduced after an initial exposure to AA. This nonresponsive state of DOR after exogenous AA was mediated by a lipoxygenase (LOX)-dependent metabolite of AA. Intraplantar carrageenan also produced transient DOR functional competence and responsiveness was also reinduced by inhibition of LOX. Thus, the DOR system expressed by peripheral sensory neurons is under dual regulation by cyclooxygenase- and LOX-dependent metabolites of AA.

Footnotes

    • Received November 11, 2014.
    • Accepted January 29, 2015.
  • This research was supported by the National Institutes of Health National Institute on Drug Abuse [Grants R01-DA24865 and T32-DA031115 (to L.C.S.)]; the National Institutes of Health National Institute of Dental and Craniofacial Research [Craniofacial Oral-biology Student Training in Academic Research Training Grant T32-DE14318]; and the William and Ella Owens Medical Research Foundation.

  • dx.doi.org/10.1124/jpet.114.221366.

  • ↵Embedded ImageThis article has supplemental material available at jpet.aspetjournals.org.

  • Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 353 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 353, Issue 1
1 Apr 2015
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Research ArticleCellular and Molecular

Arachidonic Acid Regulation of δ-Opioid Receptor Function

Laura C. Sullivan, Kelly A. Berg and William P. Clarke
Journal of Pharmacology and Experimental Therapeutics April 1, 2015, 353 (1) 44-51; DOI: https://doi.org/10.1124/jpet.114.221366

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Research ArticleCellular and Molecular

Arachidonic Acid Regulation of δ-Opioid Receptor Function

Laura C. Sullivan, Kelly A. Berg and William P. Clarke
Journal of Pharmacology and Experimental Therapeutics April 1, 2015, 353 (1) 44-51; DOI: https://doi.org/10.1124/jpet.114.221366
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