Localization of opiate and histamine H1-receptors in the primate sensory ganglia and spinal cord

Ninković, M.; Hunt, SP; Gleave, J. R. W.

doi:10.1016/0006-8993(82)91056-3

Cited by 128 publications

(36 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The first set of experiments demonstrates the presence of significant amounts of opioid peptides in peripheral inflamed Immunoreactive opioid receptors were visualized on small-diameter cutaneous nerves, consistent with studies demonstrating opioid binding (25)(26)(27) and opioid receptorspecific electrophysiological effects on sensory neurons (28)(29)(30). Conceivably, activation of these receptors can cause attenuation of the excitability of nociceptive input terminals (28)(29)(30) and/or inhibition of release of excitatory transmitters (31,32) Proc.…”

Section: Discussionsupporting

confidence: 70%

Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation.

Stein

Hassan

Przewłocki

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

507

275

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 70%

Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation.

Stein

Hassan

Przewłocki

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

507

275

View full text Add to dashboard Cite

show abstract

“…Furthermore, in view of the highly differentiated neuroanatomical and temporal regulation of the synthesis of different opioid peptides under various inflammatory conditions (Iadarola et al, 1988;Millan et al 1988;Stein et al, 1990;Przewlocka et al, 1992;Przewlocki et al, 1992), it seems unlikely that such a synthesis should initiate simultaneously for three different opioid receptor systems. Lastly, we and others have demonstrated opioid receptors on peripheral nerves under normal conditions (LaMotte et al, 1976;Fields et al, 1980;Ninkovic et al, 1982;Stein et al, 1990;Hassan et al, 1993). Therefore, we put forth an alternative hypothesis, namely, that opioid receptors are preexistent on sensory nerves but hardly accessible under normal circumstances and that the disruption of a physical barrier and a subsequent facilitated access for agonists contributes to their enhanced antinociceptive effects during the early stages of inflammation.…”

Section: Discussionmentioning

confidence: 80%

Perineurial defect and peripheral opioid analgesia in inflammation

et al. 1995

View full text Add to dashboard Cite

Opioid receptors have been demonstrated on sensory nerves in both inflamed and normal subcutaneous tissue but locally applied opioid agonists produce analgesia in inflamed tissue only. Inflammation confers a disruption of the perineurial barrier that can also be induced deliberately by hyperosmolar solutions. The present study examines at which stage of Freund's adjuvant-induced inflammation peripheral opioid analgesic effects become manifest and whether a perineurial defect contributes to the appearance of such effects. To this end we have monitored the temporal evolution of inflammatory signs (swelling, temperature, hyperalgesia) and of peripheral antinociceptive effects (by the paw pressure test) of mu-, delta-, and kappa-selective opioids. Using horseradish peroxidase histochemistry, the perineurial barrier was assessed in normal and inflamed tissue and following its artificial disruption by hyperosmolar saline and mannitol in vivo. Finally, we sought to elicit analgesia in normal tissue by the concomitant application of mannitol and receptor-selective opioids or by an extremely lipophilic opioid agonist (fentanyl). We found that peripheral opioid antinociception and perineurial leakage occur simultaneously at a very early stage (within 12 hr) of the inflammatory reaction and that both can be mimicked by the administration of hyperosmolar solutions in normal tissue. Fentanyl produced peripheral antinociception in noninflamed tissue that was potentiated by mannitol or inflammation. Our findings demonstrate that the perineurium is a crucial determinant for peripheral opioid analgesia and that the efficacy of locally applied hydrophilic or lipophilic neuromodulatory compounds can be improved dramatically by the concomitant modulation of perineurial permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…Opioid receptors have also been found on the somata of a portion of dorsal root ganglion neurones grown in primary dissociated culture (Mudge, Leeman & Fischbach, 1979;Werz & Macdonald, 1982 a, b) and on a portion of adult d.r.g. neurones in vivo (Ninkovic, Hunt & Gleave, 1982) and opioids decrease calcium entry at the somatic membrane of d.r.g. neurone (Werz & Macdonald, 1982a,b).…”

Section: Discussionmentioning

confidence: 99%

Dynorphin A decreases voltage‐dependent calcium conductance of mouse dorsal root ganglion neurones.

Macdonald¹,

Werz²

1986

The Journal of Physiology

145

View full text Add to dashboard Cite

SUMMARY1. The actions of the opioid peptides dynorphin A and (Leu)enkephalin were assessed on calcium-dependent action potentials and inward calcium currents recorded from somata of mouse dorsal root ganglion (d.r.g.) neurones grown in primary dissociated cell culture. Dynorphin A and (Leu)enkephalin decreased the duration of somatic calcium-dependent action potentials in a portion of d.r.g. neurones impaled with potassium acetate-filled micropipettes. When substantial potassium conductance was blocked by intracellular injection of caesium acetate, d.r.g. neurones continued to respond to dynorphin A but responses to (Leu)enkephalin were abolished.2. In voltage-clamp experiments, dynorphin A but not (Leu)enkephalin reduced the magnitude of inward calcium currents. Dynorphin A responses were blocked by the opiate antagonist naloxone. The dynorphin A effect was due to reduction of voltage-dependent calcium conductance since dynorphin A reduced depolarizationevoked inward currents but did not alter membrane conductance following blockade ofcalcium channels by cadmium, and because dynorphin A reduced the instantaneous current-voltage slope (chord conductance) during step commands that produced maximal activation of voltage-dependent calcium conductance.3. Dynorphin A binds with high affinity to K-opioid receptors. (Leu)enkephalin, which has affinity for both It-and s-receptors but not for K-opioid receptors, was without effect on calcium conductance. Therefore, we suggest that K-receptors are coupled to voltage-dependent calcium-channels and that binding of dynorphin A produces a decrease of calcium current.

show abstract

Localization of opiate and histamine H1-receptors in the primate sensory ganglia and spinal cord

Cited by 128 publications

References 38 publications

Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation.

Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation.

Perineurial defect and peripheral opioid analgesia in inflammation

Dynorphin A decreases voltage‐dependent calcium conductance of mouse dorsal root ganglion neurones.

Contact Info

Product

Resources

About