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Probable involvement of Ca(2+)-activated Cl(-) channels (CaCCs) in the activation of CB1 cannabinoid receptors.
Life Sci. 2013 May 02; 92(14-16):815-20.LS

Abstract

AIMS

Recently, we demonstrated that peripheral antinociception induced by δ opioid receptor is dependent of Ca(2+)-activated Cl(-) channels (CaCCs). Because opioid and cannabinoid receptors share some common mechanisms of action, our objective was to identify a possible relationship between CaCCs and the endocannabinoid system.

MAIN METHODS

To induce hyperalgesia, rat paws were treated with intraplantar prostaglandin E2 (PGE2, 2μg). Nociceptive thresholds to pressure (grams) were measured using an algesimetric apparatus 3h following injection. Probabilities were calculated using ANOVA/Bonferroni's test, and values that were less than 5% were considered to be statistically significant.

KEY FINDINGS

Administration of the cannabinoid agonist CB1 anandamide (12.5, 25 and 50μg/paw) and the cannabinoid agonist CB2 PEA (5, 10 and 20μg/paw) decreased the PGE2-induced hyperalgesia in a dose-dependent manner. The possibility of the higher doses of anandamide (50μg) and PEA (20μg) having a central or systemic effect was excluded because the administration of the drug into the contralateral paw did not elicit antinociception in the right paw. As expected, the antinociceptive effects induced by anandamide and PEA were blocked by the CB1 and CB2 receptor antagonists AM251 and AM630, respectively. The peripheral antinociception was induced by anandamide but not PEA and was dose-dependently inhibited by the CaCC blocker niflumic acid (8, 16 and 32μg).

SIGNIFICANCE

These results provide the first evidence for the involvement of CaCCs in the peripheral antinociception induced by activation of the CB1 cannabinoid receptor.

Authors+Show Affiliations

Department of Pharmacology, Institute of Biological Sciences, UFMG, Av. Antônio Carlos, 6627, 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

23123446

Citation

Romero, Thiago Roberto Lima, et al. "Probable Involvement of Ca(2+)-activated Cl(-) Channels (CaCCs) in the Activation of CB1 Cannabinoid Receptors." Life Sciences, vol. 92, no. 14-16, 2013, pp. 815-20.
Romero TR, Pacheco Dda F, Duarte ID. Probable involvement of Ca(2+)-activated Cl(-) channels (CaCCs) in the activation of CB1 cannabinoid receptors. Life Sci. 2013;92(14-16):815-20.
Romero, T. R., Pacheco, D. d. a. . F., & Duarte, I. D. (2013). Probable involvement of Ca(2+)-activated Cl(-) channels (CaCCs) in the activation of CB1 cannabinoid receptors. Life Sciences, 92(14-16), 815-20. https://doi.org/10.1016/j.lfs.2012.10.006
Romero TR, Pacheco Dda F, Duarte ID. Probable Involvement of Ca(2+)-activated Cl(-) Channels (CaCCs) in the Activation of CB1 Cannabinoid Receptors. Life Sci. 2013 May 2;92(14-16):815-20. PubMed PMID: 23123446.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Probable involvement of Ca(2+)-activated Cl(-) channels (CaCCs) in the activation of CB1 cannabinoid receptors. AU - Romero,Thiago Roberto Lima, AU - Pacheco,Daniela da Fonseca, AU - Duarte,Igor Dimitri Gama, Y1 - 2012/10/30/ PY - 2012/01/24/received PY - 2012/08/30/revised PY - 2012/10/11/accepted PY - 2012/11/6/entrez PY - 2012/11/6/pubmed PY - 2013/6/5/medline SP - 815 EP - 20 JF - Life sciences JO - Life Sci VL - 92 IS - 14-16 N2 - AIMS: Recently, we demonstrated that peripheral antinociception induced by δ opioid receptor is dependent of Ca(2+)-activated Cl(-) channels (CaCCs). Because opioid and cannabinoid receptors share some common mechanisms of action, our objective was to identify a possible relationship between CaCCs and the endocannabinoid system. MAIN METHODS: To induce hyperalgesia, rat paws were treated with intraplantar prostaglandin E2 (PGE2, 2μg). Nociceptive thresholds to pressure (grams) were measured using an algesimetric apparatus 3h following injection. Probabilities were calculated using ANOVA/Bonferroni's test, and values that were less than 5% were considered to be statistically significant. KEY FINDINGS: Administration of the cannabinoid agonist CB1 anandamide (12.5, 25 and 50μg/paw) and the cannabinoid agonist CB2 PEA (5, 10 and 20μg/paw) decreased the PGE2-induced hyperalgesia in a dose-dependent manner. The possibility of the higher doses of anandamide (50μg) and PEA (20μg) having a central or systemic effect was excluded because the administration of the drug into the contralateral paw did not elicit antinociception in the right paw. As expected, the antinociceptive effects induced by anandamide and PEA were blocked by the CB1 and CB2 receptor antagonists AM251 and AM630, respectively. The peripheral antinociception was induced by anandamide but not PEA and was dose-dependently inhibited by the CaCC blocker niflumic acid (8, 16 and 32μg). SIGNIFICANCE: These results provide the first evidence for the involvement of CaCCs in the peripheral antinociception induced by activation of the CB1 cannabinoid receptor. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/23123446/Probable_involvement_of_Ca_2+__activated_Cl____channels__CaCCs__in_the_activation_of_CB1_cannabinoid_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(12)00609-1 DB - PRIME DP - Unbound Medicine ER -