Document Detail


Removing TRPV1-expressing primary afferent neurons potentiates the spinal analgesic effect of delta-opioid agonists on mechano-nociception.
MedLine Citation:
PMID:  18579164     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Most delta-opioid receptors are located on the presynaptic terminals of primary afferent neurons in the spinal cord. However, their presence in different phenotypes of primary afferent neurons and their contribution to the analgesic effect of delta-opioid agonists are not fully known. Resiniferatoxin (RTX) is an ultra-potent transient receptor potential vanilloid type 1 channel (TRPV1) agonist and can selectively remove TRPV1-expressing primary afferent neurons. In this study, we determined the role of delta-opioid receptors expressed on TRPV1 sensory neurons in the antinociceptive effect of the delta-opioid receptor agonists [D-Pen(2),D-Pen(5)]-enkephalin and [D-Ala(2),Glu(4)]-deltorphin. Nociception was measured by testing the mechanical withdrawal threshold in the hindpaw of rats. Changes in the delta-opioid receptors were assessed using immunocytochemistry and the [(3)H]-naltrindole radioligand binding. In RTX-treated rats, the delta-opioid receptor on TRPV1-immunoreactive dorsal root ganglion neurons and afferent terminals in the spinal cord was diminished. RTX treatment also significantly reduced the maximal specific binding sites (31%) of the delta-opioid receptors in the dorsal spinal cord. Interestingly, intrathecal injection of [D-Pen(2),d-Pen(5)]-enkephalin or [D-Ala(2),Glu(4)]-deltorphin produced a large and prolonged increase in the nociceptive threshold in RTX-treated rats. These findings indicate that loss of TRPV1-expressing afferent neurons leads to a substantial reduction in presynaptic delta-opioid receptors in the spinal dorsal horn. However, the effect of delta-opioid agonists on mechano-nociception is paradoxically potentiated in the absence of TRPV1-expressing sensory neurons. This information is important to our understanding of the cellular sites and mechanisms underlying the spinal analgesic effect of delta-opioid agonists.
Authors:
Shao-Rui Chen; Hui-Lin Pan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2008-05-22
Journal Detail:
Title:  Neuropharmacology     Volume:  55     ISSN:  0028-3908     ISO Abbreviation:  Neuropharmacology     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-07-21     Completed Date:  2008-11-25     Revised Date:  2014-09-20    
Medline Journal Info:
Nlm Unique ID:  0236217     Medline TA:  Neuropharmacology     Country:  England    
Other Details:
Languages:  eng     Pagination:  215-22     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Analgesics, Opioid / pharmacology
Analysis of Variance
Animals
Behavior, Animal / drug effects
Diterpenes / pharmacology
Dose-Response Relationship, Drug
Enkephalin, D-Penicillamine (2,5)- / pharmacology
Gene Expression Regulation / drug effects
Hyperalgesia / drug therapy*
Male
Naltrexone / analogs & derivatives,  metabolism
Oligopeptides / pharmacology
Pain Threshold / drug effects*
Protein Binding / drug effects
Rats
Rats, Sprague-Dawley
Receptors, Opioid, delta / agonists*,  metabolism
Sensory Receptor Cells / drug effects,  metabolism*
Spinal Cord / pathology*
TRPV Cation Channels / agonists,  metabolism*
Tritium / metabolism
Grant Support
ID/Acronym/Agency:
GM64830/GM/NIGMS NIH HHS; NS45602/NS/NINDS NIH HHS; R01 GM064830/GM/NIGMS NIH HHS; R01 GM064830-05A2/GM/NIGMS NIH HHS; R01 NS045602/NS/NINDS NIH HHS; R01 NS045602-05/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Analgesics, Opioid; 0/Diterpenes; 0/Oligopeptides; 0/Receptors, Opioid, delta; 0/TRPV Cation Channels; 0/Trpv1 protein, rat; 10028-17-8/Tritium; 111555-53-4/naltrindole; 122752-16-3/deltorphin II, Ala(2)-; 5S6W795CQM/Naltrexone; 88373-73-3/Enkephalin, D-Penicillamine (2,5)-; A5O6P1UL4I/resiniferatoxin
Comments/Corrections

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