Open AccessTRPV1 in Brain Is Involved in Acetaminophen-Induced Antinociception
Author(s) -
Christophe Mallet,
David André Barrière,
Anna Ermund,
Bo Jönsson,
Alain Eschalier,
Peter M. Zygmunt,
Edward D. Högestätt
Publication year - 2010
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0012748
Subject(s) - trpv , pharmacology , chemistry , endocannabinoid system , fatty acid amide hydrolase , acetaminophen , trpv1 , nociception , biochemistry , medicine , cannabinoid receptor , agonist , transient receptor potential channel , receptor
Acetaminophen, the major active metabolite of acetanilide in man, has become one of the most popular over-the-counter analgesic and antipyretic agents, consumed by millions of people daily. However, its mechanism of action is still a matter of debate. We have previously shown that acetaminophen is further metabolized to N-(4-hydroxyphenyl)-5Z,8Z,11Z,14Z -eicosatetraenamide (AM404) by fatty acid amide hydrolase (FAAH) in the rat and mouse brain and that this metabolite is a potent activator of transient receptor potential vanilloid 1 (TRPV(1)) in vitro. Pharmacological activation of TRPV(1) in the midbrain periaqueductal gray elicits antinociception in rats. It is therefore possible that activation of TRPV(1) in the brain contributes to the analgesic effect of acetaminophen.
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