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Fatty acid amide hydrolase blockade attenuates the development of collagen-induced arthritis and related thermal hyperalgesia in mice.
Pharmacol Biochem Behav. 2011 Oct; 99(4):718-25.PB

Abstract

Fatty acid amide hydrolase (FAAH) is the primary degradative enzyme of the endocannabinoid anandamide (N-arachidonoylethanolamine), which activates cannabinoid CB(1) and CB(2) receptors. FAAH disruption reduces nociception in a variety of acute rodent models of inflammatory pain. The present study investigated whether these actions extend to the chronic, collagen-induced arthritis (CIA) model. We investigated the anti-arthritic and anti-hyperalgesic effects of genetic deletion or pharmacological inhibition of FAAH in the CIA model. FAAH (-/-) mice, and FAAH-NS mice that express FAAH exclusively in nervous tissue, displayed decreased severity of CIA and associated hyperalgesia. These phenotypic anti-arthritic effects were prevented by repeated daily injections of the CB(2) receptor antagonist, SR144528, but not the CB(1) receptor antagonist rimonabant. Similarly, repeated administration of the FAAH inhibitor URB597 reduced CIA severity, and acute administration of rimonabant, but not SR144528, blocked the anti-hyperalgesic effects of prolonged FAAH inhibition, suggesting that prolonged CB(2) receptor activation reduces the severity of CIA, whereas acute CB(1) receptor activation reduces CIA-induced hyperalgesia. In contrast, acute administration of URB597 elicited a CB(1) receptor-dependent anti-hyperalgesic effect. The observed anti-arthritic and anti-hyperalgesic properties of FAAH inhibition, coupled with a lack of apparent behavioral alterations, suggest that endocannabinoid modulating enzymes offer a promising therapeutic target for the development of novel pharmacological approaches to treat rheumatoid arthritis and associated hyperalgesia.

Authors+Show Affiliations

Department of Psychology, West Virginia University, Morgantown, WV 26506, USA. steven.kinsey@mail.wvu.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

21740924

Citation

Kinsey, Steven G., et al. "Fatty Acid Amide Hydrolase Blockade Attenuates the Development of Collagen-induced Arthritis and Related Thermal Hyperalgesia in Mice." Pharmacology, Biochemistry, and Behavior, vol. 99, no. 4, 2011, pp. 718-25.
Kinsey SG, Naidu PS, Cravatt BF, et al. Fatty acid amide hydrolase blockade attenuates the development of collagen-induced arthritis and related thermal hyperalgesia in mice. Pharmacol Biochem Behav. 2011;99(4):718-25.
Kinsey, S. G., Naidu, P. S., Cravatt, B. F., Dudley, D. T., & Lichtman, A. H. (2011). Fatty acid amide hydrolase blockade attenuates the development of collagen-induced arthritis and related thermal hyperalgesia in mice. Pharmacology, Biochemistry, and Behavior, 99(4), 718-25. https://doi.org/10.1016/j.pbb.2011.06.022
Kinsey SG, et al. Fatty Acid Amide Hydrolase Blockade Attenuates the Development of Collagen-induced Arthritis and Related Thermal Hyperalgesia in Mice. Pharmacol Biochem Behav. 2011;99(4):718-25. PubMed PMID: 21740924.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fatty acid amide hydrolase blockade attenuates the development of collagen-induced arthritis and related thermal hyperalgesia in mice. AU - Kinsey,Steven G, AU - Naidu,Pattipati S, AU - Cravatt,Benjamin F, AU - Dudley,David T, AU - Lichtman,Aron H, Y1 - 2011/06/29/ PY - 2011/04/29/received PY - 2011/06/03/revised PY - 2011/06/18/accepted PY - 2011/7/12/entrez PY - 2011/7/12/pubmed PY - 2011/12/14/medline SP - 718 EP - 25 JF - Pharmacology, biochemistry, and behavior JO - Pharmacol. Biochem. Behav. VL - 99 IS - 4 N2 - Fatty acid amide hydrolase (FAAH) is the primary degradative enzyme of the endocannabinoid anandamide (N-arachidonoylethanolamine), which activates cannabinoid CB(1) and CB(2) receptors. FAAH disruption reduces nociception in a variety of acute rodent models of inflammatory pain. The present study investigated whether these actions extend to the chronic, collagen-induced arthritis (CIA) model. We investigated the anti-arthritic and anti-hyperalgesic effects of genetic deletion or pharmacological inhibition of FAAH in the CIA model. FAAH (-/-) mice, and FAAH-NS mice that express FAAH exclusively in nervous tissue, displayed decreased severity of CIA and associated hyperalgesia. These phenotypic anti-arthritic effects were prevented by repeated daily injections of the CB(2) receptor antagonist, SR144528, but not the CB(1) receptor antagonist rimonabant. Similarly, repeated administration of the FAAH inhibitor URB597 reduced CIA severity, and acute administration of rimonabant, but not SR144528, blocked the anti-hyperalgesic effects of prolonged FAAH inhibition, suggesting that prolonged CB(2) receptor activation reduces the severity of CIA, whereas acute CB(1) receptor activation reduces CIA-induced hyperalgesia. In contrast, acute administration of URB597 elicited a CB(1) receptor-dependent anti-hyperalgesic effect. The observed anti-arthritic and anti-hyperalgesic properties of FAAH inhibition, coupled with a lack of apparent behavioral alterations, suggest that endocannabinoid modulating enzymes offer a promising therapeutic target for the development of novel pharmacological approaches to treat rheumatoid arthritis and associated hyperalgesia. SN - 1873-5177 UR - https://www.unboundmedicine.com/medline/citation/21740924/Fatty_acid_amide_hydrolase_blockade_attenuates_the_development_of_collagen_induced_arthritis_and_related_thermal_hyperalgesia_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-3057(11)00221-8 DB - PRIME DP - Unbound Medicine ER -