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Cannabinoid modulation of cutaneous Adelta nociceptors during inflammation.
J Neurophysiol. 2008 Nov; 100(5):2794-806.JN

Abstract

Previous studies have demonstrated that locally administered cannabinoids attenuate allodynia and hyperalgesia through activation of peripheral cannabinoid receptors (CB(1) and CB(2)). However, it is currently unknown if cannabinoids alter the response properties of nociceptors. In the present study, correlative behavioral and in vivo electrophysiological studies were conducted to determine if peripheral administration of the cannabinoid receptor agonists arachidonyl-2'-chloroethylamide (ACEA) or (R)-(+)-methanandamide (methAEA) could attenuate mechanical allodynia and hyperalgesia, and decrease mechanically evoked responses of Adelta nociceptors. Twenty-four hours after intraplantar injection of complete Freund's adjuvant (CFA), rats exhibited allodynia (decrease in paw withdrawal threshold) and hyperalgesia (increase in paw withdrawal frequency), which were attenuated by both ACEA and methAEA. The antinociceptive effects of these cannabinoids were blocked by co-administration with the CB(1) receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophen yl)-4-methyl-1H-pyrazole-3-carboxamide (AM251) but not with the CB(2) receptor antagonist 6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-y l](4-methoxyphenyl)methanone (AM630). ACEA and methAEA did not produce antinociception under control, non-inflamed conditions 24 h after intraplantar injection of saline. In parallel studies, recordings were made from cutaneous Adelta nociceptors from inflamed or control, non-inflamed skin. Both ACEA and methAEA decreased responses evoked by mechanical stimulation of Adelta nociceptors from inflamed skin but not from non-inflamed skin, and this decrease was blocked by administration of the CB(1) receptor antagonist AM251. These results suggest that attenuation of mechanically evoked responses of Adelta nociceptors contributes to the behavioral antinociception produced by activation of peripheral CB(1) receptors during inflammation.

Authors+Show Affiliations

Department of Diagnostic and Biological Sciences, University of Minnesota School of Dentistry, 515 Delaware St. SE, 17-252 Moos Tower, Minneapolis, MN 55455, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18784270

Citation

Potenzieri, Carl, et al. "Cannabinoid Modulation of Cutaneous Adelta Nociceptors During Inflammation." Journal of Neurophysiology, vol. 100, no. 5, 2008, pp. 2794-806.
Potenzieri C, Brink TS, Pacharinsak C, et al. Cannabinoid modulation of cutaneous Adelta nociceptors during inflammation. J Neurophysiol. 2008;100(5):2794-806.
Potenzieri, C., Brink, T. S., Pacharinsak, C., & Simone, D. A. (2008). Cannabinoid modulation of cutaneous Adelta nociceptors during inflammation. Journal of Neurophysiology, 100(5), 2794-806. https://doi.org/10.1152/jn.90809.2008
Potenzieri C, et al. Cannabinoid Modulation of Cutaneous Adelta Nociceptors During Inflammation. J Neurophysiol. 2008;100(5):2794-806. PubMed PMID: 18784270.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cannabinoid modulation of cutaneous Adelta nociceptors during inflammation. AU - Potenzieri,Carl, AU - Brink,Thaddeus S, AU - Pacharinsak,Cholawat, AU - Simone,Donald A, Y1 - 2008/09/10/ PY - 2008/9/12/pubmed PY - 2009/4/21/medline PY - 2008/9/12/entrez SP - 2794 EP - 806 JF - Journal of neurophysiology JO - J Neurophysiol VL - 100 IS - 5 N2 - Previous studies have demonstrated that locally administered cannabinoids attenuate allodynia and hyperalgesia through activation of peripheral cannabinoid receptors (CB(1) and CB(2)). However, it is currently unknown if cannabinoids alter the response properties of nociceptors. In the present study, correlative behavioral and in vivo electrophysiological studies were conducted to determine if peripheral administration of the cannabinoid receptor agonists arachidonyl-2'-chloroethylamide (ACEA) or (R)-(+)-methanandamide (methAEA) could attenuate mechanical allodynia and hyperalgesia, and decrease mechanically evoked responses of Adelta nociceptors. Twenty-four hours after intraplantar injection of complete Freund's adjuvant (CFA), rats exhibited allodynia (decrease in paw withdrawal threshold) and hyperalgesia (increase in paw withdrawal frequency), which were attenuated by both ACEA and methAEA. The antinociceptive effects of these cannabinoids were blocked by co-administration with the CB(1) receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophen yl)-4-methyl-1H-pyrazole-3-carboxamide (AM251) but not with the CB(2) receptor antagonist 6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-y l](4-methoxyphenyl)methanone (AM630). ACEA and methAEA did not produce antinociception under control, non-inflamed conditions 24 h after intraplantar injection of saline. In parallel studies, recordings were made from cutaneous Adelta nociceptors from inflamed or control, non-inflamed skin. Both ACEA and methAEA decreased responses evoked by mechanical stimulation of Adelta nociceptors from inflamed skin but not from non-inflamed skin, and this decrease was blocked by administration of the CB(1) receptor antagonist AM251. These results suggest that attenuation of mechanically evoked responses of Adelta nociceptors contributes to the behavioral antinociception produced by activation of peripheral CB(1) receptors during inflammation. SN - 0022-3077 UR - https://www.unboundmedicine.com/medline/citation/18784270/Cannabinoid_modulation_of_cutaneous_Adelta_nociceptors_during_inflammation_ L2 - https://journals.physiology.org/doi/10.1152/jn.90809.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -