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Peripheral antinociception induced by δ-opioid receptors activation, but not μ- or κ-, is mediated by Ca²⁺-activated Cl⁻ channels.
Eur J Pharmacol. 2012 Jan 15; 674(2-3):255-9.EJ

Abstract

Studies have demonstrated that the L-arginine/NO/cGMP pathway and the potassium and calcium channels are involved in the mechanisms underlying opioid receptor activation. As additional pathways may participate in the observed antinociceptive effects following opioid exposure, the aim of our study was to determine whether Ca(2+)-activated Cl(-) channels (CaCCs) are involved in peripheral antinociception induced by μ-, δ- and κ-opioid receptor activation. Hyperalgesia was induced by intraplantar injection of prostaglandin E(2) (PGE(2), 2 μg). Nociceptive thresholds to pressure (grams) were measured using an algesimetric apparatus 3h following injection. The μ-opioid receptor agonist morphine (200 μg), δ-opioid receptor agonist (+)-4-[(alphaR)-alpha-((2S,5R)-4-Allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethylbenzamide (SNC80, 80 μg), κ-opioid receptor agonist bremazocine (50 μg), CaCCs blocker niflumic acid (8-64 μg), CaCCs blocker 5-Nitro-2-(3-phenylpropylamino) benzoic acid (NPPB, 32-128 μg), nitric oxide donor sodium nitroprusside (SNP, 500 μg) and cGMP exogenous analogs dibutyryl cGMP (db-cGMP, 100 μg) were also administered into the paw. The CaCCs blocker niflumic acid and NPPB partially reversed the peripheral antinociception induced by exposure to the SNC80 in a dose-dependent manner. In contrast, niflumic acid did not modify the antinociceptive effect observed following exposure to morphine or bremazocine. Additionally, the peripheral antinociception induced by the NO donor SNP or by db-cGMP was not inhibited by niflumic acid. These results provide evidence for the involvement of CaCCs in the peripheral antinociception induced by SNC80. CaCCs activation does not appear to be involved when μ- and κ-opioid receptors are activated. In addition, we did not observe a link between CaCCs and the L-arginine/NO/GMPc pathway.

Authors+Show Affiliations

Department of Pharmacology, Institute of Biological Sciences, UFMG, Av. Antônio Carlos, 6627, CEP: 31.270.100, Belo Horizonte, Brazil.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22134006

Citation

Pacheco, Daniela da Fonseca, et al. "Peripheral Antinociception Induced By Δ-opioid Receptors Activation, but Not Μ- or Κ-, Is Mediated By Ca²⁺-activated Cl⁻ Channels." European Journal of Pharmacology, vol. 674, no. 2-3, 2012, pp. 255-9.
Pacheco Dda F, Pacheco CM, Duarte ID. Peripheral antinociception induced by δ-opioid receptors activation, but not μ- or κ-, is mediated by Ca²⁺-activated Cl⁻ channels. Eur J Pharmacol. 2012;674(2-3):255-9.
Pacheco, D. d. a. . F., Pacheco, C. M., & Duarte, I. D. (2012). Peripheral antinociception induced by δ-opioid receptors activation, but not μ- or κ-, is mediated by Ca²⁺-activated Cl⁻ channels. European Journal of Pharmacology, 674(2-3), 255-9. https://doi.org/10.1016/j.ejphar.2011.11.023
Pacheco Dda F, Pacheco CM, Duarte ID. Peripheral Antinociception Induced By Δ-opioid Receptors Activation, but Not Μ- or Κ-, Is Mediated By Ca²⁺-activated Cl⁻ Channels. Eur J Pharmacol. 2012 Jan 15;674(2-3):255-9. PubMed PMID: 22134006.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peripheral antinociception induced by δ-opioid receptors activation, but not μ- or κ-, is mediated by Ca²⁺-activated Cl⁻ channels. AU - Pacheco,Daniela da Fonseca, AU - Pacheco,Cinthia Mara da Fonseca, AU - Duarte,Igor Dimitri Gama, Y1 - 2011/11/27/ PY - 2011/08/03/received PY - 2011/11/03/revised PY - 2011/11/10/accepted PY - 2011/12/3/entrez PY - 2011/12/3/pubmed PY - 2012/5/4/medline SP - 255 EP - 9 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 674 IS - 2-3 N2 - Studies have demonstrated that the L-arginine/NO/cGMP pathway and the potassium and calcium channels are involved in the mechanisms underlying opioid receptor activation. As additional pathways may participate in the observed antinociceptive effects following opioid exposure, the aim of our study was to determine whether Ca(2+)-activated Cl(-) channels (CaCCs) are involved in peripheral antinociception induced by μ-, δ- and κ-opioid receptor activation. Hyperalgesia was induced by intraplantar injection of prostaglandin E(2) (PGE(2), 2 μg). Nociceptive thresholds to pressure (grams) were measured using an algesimetric apparatus 3h following injection. The μ-opioid receptor agonist morphine (200 μg), δ-opioid receptor agonist (+)-4-[(alphaR)-alpha-((2S,5R)-4-Allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethylbenzamide (SNC80, 80 μg), κ-opioid receptor agonist bremazocine (50 μg), CaCCs blocker niflumic acid (8-64 μg), CaCCs blocker 5-Nitro-2-(3-phenylpropylamino) benzoic acid (NPPB, 32-128 μg), nitric oxide donor sodium nitroprusside (SNP, 500 μg) and cGMP exogenous analogs dibutyryl cGMP (db-cGMP, 100 μg) were also administered into the paw. The CaCCs blocker niflumic acid and NPPB partially reversed the peripheral antinociception induced by exposure to the SNC80 in a dose-dependent manner. In contrast, niflumic acid did not modify the antinociceptive effect observed following exposure to morphine or bremazocine. Additionally, the peripheral antinociception induced by the NO donor SNP or by db-cGMP was not inhibited by niflumic acid. These results provide evidence for the involvement of CaCCs in the peripheral antinociception induced by SNC80. CaCCs activation does not appear to be involved when μ- and κ-opioid receptors are activated. In addition, we did not observe a link between CaCCs and the L-arginine/NO/GMPc pathway. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/22134006/Peripheral_antinociception_induced_by_δ_opioid_receptors_activation_but_not_μ__or_κ__is_mediated_by_Ca²⁺_activated_Cl⁻_channels_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(11)01475-0 DB - PRIME DP - Unbound Medicine ER -