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Selective activation of cannabinoid CB2 receptors suppresses hyperalgesia evoked by intradermal capsaicin.
J Pharmacol Exp Ther 2004; 308(2):446-53JP

Abstract

The present studies were conducted to test the hypothesis that activation of peripheral cannabinoid CB(2) receptors would suppress hyperalgesia evoked by intradermal administration of capsaicin, the pungent ingredient in hot chili peppers. The CB(2)-selective cannabinoid agonist (2-iodo-5-nitro-phenyl)-[1-(1-methyl-piperidin-2-ylmethyl)-1H-indol-3-yl]-methanone (AM1241) (33, 330 microg/kg i.p.) suppressed the development of capsaicin-evoked thermal and mechanical hyperalgesia and allodynia. AM1241 also produced a dose-dependent suppression of capsaicin-evoked nocifensive behavior. The AM1241-induced suppression of each parameter of capsaicin-evoked pain behavior was completely blocked by the CB(2) antagonist N-[(1S)-endo-1,3,3-trimethyl bicycle [2.2.1] heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528) but not by the CB(1) antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamidehydrochloride (SR141716A). AM1241 (33 microg/kg i.pl.) suppressed capsaicin-evoked thermal and mechanical hyperalgesia and allodynia after local administration to the capsaicin-treated (ipsilateral) paw but was inactive after administration to the capsaicin-untreated (contralateral) paw. Our data indicate that AM1241 suppresses capsaicin-evoked hyperalgesia and allodynia through a local site of action. These data provide evidence that actions at cannabinoid CB(2) receptors are sufficient to normalize nociceptive thresholds and produce antinociception in persistent pain states.

Authors+Show Affiliations

Neuroscience and Behavior Program, Department of Psychology, University of Georgia, Athens, GA 30602-3013, USA. ahomann@uga.edu

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

14610224

Citation

Hohmann, Andrea G., et al. "Selective Activation of Cannabinoid CB2 Receptors Suppresses Hyperalgesia Evoked By Intradermal Capsaicin." The Journal of Pharmacology and Experimental Therapeutics, vol. 308, no. 2, 2004, pp. 446-53.
Hohmann AG, Farthing JN, Zvonok AM, et al. Selective activation of cannabinoid CB2 receptors suppresses hyperalgesia evoked by intradermal capsaicin. J Pharmacol Exp Ther. 2004;308(2):446-53.
Hohmann, A. G., Farthing, J. N., Zvonok, A. M., & Makriyannis, A. (2004). Selective activation of cannabinoid CB2 receptors suppresses hyperalgesia evoked by intradermal capsaicin. The Journal of Pharmacology and Experimental Therapeutics, 308(2), pp. 446-53.
Hohmann AG, et al. Selective Activation of Cannabinoid CB2 Receptors Suppresses Hyperalgesia Evoked By Intradermal Capsaicin. J Pharmacol Exp Ther. 2004;308(2):446-53. PubMed PMID: 14610224.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selective activation of cannabinoid CB2 receptors suppresses hyperalgesia evoked by intradermal capsaicin. AU - Hohmann,Andrea G, AU - Farthing,Jesse N, AU - Zvonok,Alexander M, AU - Makriyannis,Alexandros, Y1 - 2003/11/10/ PY - 2003/11/12/pubmed PY - 2004/3/12/medline PY - 2003/11/12/entrez SP - 446 EP - 53 JF - The Journal of pharmacology and experimental therapeutics JO - J. Pharmacol. Exp. Ther. VL - 308 IS - 2 N2 - The present studies were conducted to test the hypothesis that activation of peripheral cannabinoid CB(2) receptors would suppress hyperalgesia evoked by intradermal administration of capsaicin, the pungent ingredient in hot chili peppers. The CB(2)-selective cannabinoid agonist (2-iodo-5-nitro-phenyl)-[1-(1-methyl-piperidin-2-ylmethyl)-1H-indol-3-yl]-methanone (AM1241) (33, 330 microg/kg i.p.) suppressed the development of capsaicin-evoked thermal and mechanical hyperalgesia and allodynia. AM1241 also produced a dose-dependent suppression of capsaicin-evoked nocifensive behavior. The AM1241-induced suppression of each parameter of capsaicin-evoked pain behavior was completely blocked by the CB(2) antagonist N-[(1S)-endo-1,3,3-trimethyl bicycle [2.2.1] heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528) but not by the CB(1) antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamidehydrochloride (SR141716A). AM1241 (33 microg/kg i.pl.) suppressed capsaicin-evoked thermal and mechanical hyperalgesia and allodynia after local administration to the capsaicin-treated (ipsilateral) paw but was inactive after administration to the capsaicin-untreated (contralateral) paw. Our data indicate that AM1241 suppresses capsaicin-evoked hyperalgesia and allodynia through a local site of action. These data provide evidence that actions at cannabinoid CB(2) receptors are sufficient to normalize nociceptive thresholds and produce antinociception in persistent pain states. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/14610224/Selective_activation_of_cannabinoid_CB2_receptors_suppresses_hyperalgesia_evoked_by_intradermal_capsaicin_ L2 - http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=14610224 DB - PRIME DP - Unbound Medicine ER -