Cited by 328Cannabis and Cannabinoid ResearchPain Mechanisms and TreatmentsInflammatory mediators and NSAID effects

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Mice lacking fatty acid amide hydrolase exhibit a cannabinoid receptor-mediated phenotypic hypoalgesia

Lichtman, Aron H, Shelton, Christopher C, Advani, Tushar, Cravatt, Benjamin F·2004·Pain

DOI 10.1016/j.pain.2004.01.022

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Abstract

Although the N-arachidonoyl ethanolamine (anandamide) binds to cannabinoid receptors and has been implicated in the suppression of pain, its rapid catabolism in vivo by fatty acid amide hydrolase (FAAH) has presented a challenge in investigating the physiological functions of this endogenous cannabinoid. In order to test whether anandamide and other non-cannabinoid fatty amides modulate nociception, we compared FAAH (+/+) and (-/-) mice in the tail immersion, hot plate, and formalin tests, as well as for thermal hyperalgesia in the carrageenan and the chronic constriction injury (CCI) models. FAAH (-/-) mice exhibited a CB1 receptor-mediated phenotypic hypoalgesia in thermal nociceptive tests. These mice also exhibited CB1 receptor-mediated hypoalgesia in both phases of the formalin test accompanied with a phenotypic anti-edema effect, which was not blocked by either CB1 or CB2 antagonists. Additionally, FAAH (-/-) mice displayed thermal anti-hyperalgesic and anti-inflammatory effects in the carrageenan model that were mediated, in part, by CB2, but not CB1 receptors. In contrast, no genotype differences in pain behavior were evident following CCI, which was instead found to obliterate the phenotypic hypoalgesia displayed by FAAH (-/-) mice in the tail immersion and hot plate tests, suggesting that nerve injury may promote adaptive changes in these animals. Collectively, these findings demonstrate a cannabinoid receptor-mediated analgesic phenotype in FAAH (-/-) mice. In more general terms, these findings suggest that selective inhibitors of FAAH might represent a viable pharmacological approach for the clinical treatment of pain disorders.

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Authors: Lichtman, A. H., Shelton, C. C., Advani, T., & Cravatt, B. F.
Affiliations: Scripps Research Institute (US)
Virginia Commonwealth University (US)
Corresponding author: Lichtman, Aron H
ORCID: Lichtman, Aron H
Cravatt, Benjamin F
Venue: Pain
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2004-06
Volume: 109
Issue: 3
Pages: 319-327
ISSN: 0304-3959 (ISSN-L)
DOI: 10.1016/j.pain.2004.01.022
OpenAlex: W2094469214
Cited by: 301
References: 53
Citations by year: 2026: 3 · 2025: 4 · 2024: 2 · 2023: 5 · 2022: 6 · 2021: 2 · 2020: 8 · 2019: 5 · 2018: 10 · 2017: 8 · 2016: 7 · 2015: 14 · 2014: 21 · 2013: 14 · 2012: 23
FWCI: 17.17
Type: journal article
Language: en
Open access: closed
Locations: Pain (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute on Drug Abuse (DA015197, P01DA009789, R01DA015197, DA‐03672, DA 09789)
Topics: Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
Keywords: fatty acid amide hydrolase, anandamide, endocannabinoid system, CB1 receptor, CB2 receptor, thermal hyperalgesia, formalin test, chronic constriction injury, nerve injury, analgesic effect, FAAH inhibitors
MeSH terms: Fatty Acid Amide Hydrolases, Adaptation, Physiological, Amidohydrolases, Animals, Arachidonic Acids, Disease Models, Animal, Enzyme Inhibitors, Female, Genotype, Inflammation, Male, Pain, Pain Measurement, Peripheral Nerves, Phenotype, Pain Threshold, Mice, Knockout, Somatosensory Disorders, Receptors, Cannabinoid, Receptor, Cannabinoid, CB1, Receptor, Cannabinoid, CB2, Mice, Polyunsaturated Alkamides, Peripheral Nerve Injuries, Cannabinoid Receptor Antagonists, Endocannabinoids

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Mice lacking fatty acid amide hydrolase exhibit a cannabinoid receptor-mediated phenotypic hypoalgesia

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