All Relations between fatty acid amide hydrolase and cannabinoids

Publication Sentence Publish Date Extraction Date Species
Yury M Morozov, Yezekiel Ben-Ari, Tamas F Freun. The spatial and temporal pattern of fatty acid amide hydrolase expression in rat hippocampus during postnatal development. The European journal of neuroscience. vol 20. issue 2. 2004-09-30. PMID:15233754. during postnatal development of the hippocampus, the spatio-temporal expression of faah correlates well with the general pattern of neuronal maturation, but not with the arrival of afferent pathways, which suggests that faah - and its major endocannabinoid substrate, anandamide - is unlikely to be involved in the presynaptic control of neurotransmission. 2004-09-30 2023-08-12 rat
Christopher S Breivogel, J Michael Walker, Susan M Huang, Mary Beth Roy, Steven R Childer. Cannabinoid signaling in rat cerebellar granule cells: G-protein activation, inhibition of glutamate release and endogenous cannabinoids. Neuropharmacology. vol 47. issue 1. 2004-09-21. PMID:15165836. the fatty acid amide hydrolase (faah) inhibitor phenylmethylsulfonyl fluoride (pmsf) and the anandamide uptake inhibitor am404 inhibited transmitter release, implying that the antagonist effects were mediated by blockade of endocannabinoid activity. 2004-09-21 2023-08-12 rat
Jimok Kim, Bradley E Alge. Inhibition of cyclooxygenase-2 potentiates retrograde endocannabinoid effects in hippocampus. Nature neuroscience. vol 7. issue 7. 2004-09-14. PMID:15184902. here we show that inhibition of cyclooxygenase-2 (cox-2), not fatty acid amide hydrolase (faah), prolongs dsi, suggesting that cox-2 limits endocannabinoid action. 2004-09-14 2023-08-12 Not clear
Benjamin F Cravatt, Alan Saghatelian, Edward G Hawkins, Angela B Clement, Michael H Bracey, Aron H Lichtma. Functional disassociation of the central and peripheral fatty acid amide signaling systems. Proceedings of the National Academy of Sciences of the United States of America. vol 101. issue 29. 2004-08-26. PMID:15247426. this anatomically restricted biochemical phenotype correlated with a reversion of the reduced pain sensitivity of faah(-/-) mice, consistent with the faa anandamide producing this effect by acting on cannabinoid receptors in the nervous system. 2004-08-26 2023-08-12 mouse
John C Ashton, Ian Appleton, Cynthia L Darlington, Paul F Smit. Cannabinoid CB1 receptor protein expression in the rat choroid plexus: a possible involvement of cannabinoids in the regulation of cerebrospinal fluid. Neuroscience letters. vol 364. issue 1. 2004-08-23. PMID:15193752. cannabinoid cb1 receptors in the brain are expressed on axon terminals presynaptic to neurons that express fatty acid amide hydrolase (faah). 2004-08-23 2023-08-12 rat
D Fegley, S Kathuria, R Mercier, C Li, A Goutopoulos, A Makriyannis, D Piomell. Anandamide transport is independent of fatty-acid amide hydrolase activity and is blocked by the hydrolysis-resistant inhibitor AM1172. Proceedings of the National Academy of Sciences of the United States of America. vol 101. issue 23. 2004-08-17. PMID:15138300. moreover, systemic administration of am404 to either wild-type or faah(-/-) mice enhanced the hypothermic effects of exogenous anandamide, a response that was prevented by the cb(1) cannabinoid antagonist rimonabant (sr141716a). 2004-08-17 2023-08-12 mouse
Silvia Ortega-Gutiérrez, E Gregory Hawkins, Alma Viso, María L López-Rodríguez, Benjamin F Cravat. Comparison of anandamide transport in FAAH wild-type and knockout neurons: evidence for contributions by both FAAH and the CB1 receptor to anandamide uptake. Biochemistry. vol 43. issue 25. 2004-08-17. PMID:15209515. collectively, these results indicate that the protein-dependent uptake of aea is largely mediated by known constituents of the endocannabinoid system (faah and the cb1 receptor), although a partial contribution of an additional ucm707-sensitive protein is also suggested. 2004-08-17 2023-08-12 mouse
Silvana Gaetani, Vincenzo Cuomo, Daniele Piomell. Anandamide hydrolysis: a new target for anti-anxiety drugs? Trends in molecular medicine. vol 9. issue 11. 2004-08-12. PMID:14604824. pharmacological blockade of the enzyme fatty acid amide hydrolase (faah), which is responsible for intracellular anandamide degradation, produces anxiolytic-like effects in rats without causing the wide spectrum of behavioral responses typical of direct-acting cannabinoid agonists. 2004-08-12 2023-08-12 rat
John M McPartlan. Phylogenomic and chemotaxonomic analysis of the endocannabinoid system. Brain research. Brain research reviews. vol 45. issue 1. 2004-06-28. PMID:15063097. the endocannabinoid system consists of two cannabinoid (cb) receptors, seven ligands, and ligand-catabolizing enzymes such as fatty acid amid hydrolase (faah) and monoglyceride lipase (mgl). 2004-06-28 2023-08-12 Not clear
John M McPartlan. Phylogenomic and chemotaxonomic analysis of the endocannabinoid system. Brain research. Brain research reviews. vol 45. issue 1. 2004-06-28. PMID:15063097. from an evolutionary perspective it appears that (1) endocannabinoid ligands evolved before cb receptors; (2) the ligands evolved independently multiple times; (3) cb receptors evolved prior to the metazoan-bilaterian divergence (ie, between extant hydra and leech), but were secondarily lost in the ecdysozoa; (4) vr1 may predate cb receptors but its affinity for endocannabinoids is a recent acquisition, appearing after the lower vertebrate-mammal divergence; (5) mgl may be as old as the ligands, whereas faah evolved recently, after the appearance of vertebrates. 2004-06-28 2023-08-12 Not clear
John M McPartlan. Phylogenomic and chemotaxonomic analysis of the endocannabinoid system. Brain research. Brain research reviews. vol 45. issue 1. 2004-06-28. PMID:15063097. linking faah, vr1, and anandamide implies a coupling among the remaining "older" parts of the endocannabinoid system, mgl, cb receptors, and 2-ag. 2004-06-28 2023-08-12 Not clear
I Matias, J Chen, L De Petrocellis, T Bisogno, A Ligresti, F Fezza, A H-P Krauss, L Shi, C E Protzman, C Li, Y Liang, A L Nieves, K M Kedzie, R M Burk, V Di Marzo, D F Woodwar. Prostaglandin ethanolamides (prostamides): in vitro pharmacology and metabolism. The Journal of pharmacology and experimental therapeutics. vol 309. issue 2. 2004-06-21. PMID:14757851. we investigated whether prostaglandin ethanolamides (prostamides) e(2), f(2alpha), and d(2) exert some of their effects by 1) activating prostanoid receptors either per se or after conversion into the corresponding prostaglandins; 2) interacting with proteins for the inactivation of the endocannabinoid n-arachidonoylethanolamide (aea), for example fatty acid amide hydrolase (faah), thereby enhancing aea endogenous levels; or 3) activating the vanilloid receptor type-1 (trpv1). 2004-06-21 2023-08-12 human
Yoffi Segall, Gary B Quistad, Daniel K Nomura, John E Casid. Arachidonylsulfonyl derivatives as cannabinoid CB1 receptor and fatty acid amide hydrolase inhibitors. Bioorganic & medicinal chemistry letters. vol 13. issue 19. 2004-05-03. PMID:12951114. arachidonylsulfonyl derivatives as cannabinoid cb1 receptor and fatty acid amide hydrolase inhibitors. 2004-05-03 2023-08-12 mouse
Yoffi Segall, Gary B Quistad, Daniel K Nomura, John E Casid. Arachidonylsulfonyl derivatives as cannabinoid CB1 receptor and fatty acid amide hydrolase inhibitors. Bioorganic & medicinal chemistry letters. vol 13. issue 19. 2004-05-03. PMID:12951114. arachidonylsulfonyl fluoride (3), reported here for the first time, is similar in potency to its known methyl arachidonylfluorophosphonate (2) analogue as an inhibitor of mouse brain fatty acid amide hydrolase activity (ic(50) 0.1 nm) and cannabinoid cb1 agonist [3h]cp 55,940 binding (ic(50) 304-530 nm). 2004-05-03 2023-08-12 mouse
Maria Grazia Cascio, Alberto Minassi, Alessia Ligresti, Giovanni Appendino, Sumner Burstein, Vincenzo Di Marz. A structure-activity relationship study on N-arachidonoyl-amino acids as possible endogenous inhibitors of fatty acid amide hydrolase. Biochemical and biophysical research communications. vol 314. issue 1. 2004-04-19. PMID:14715265. nagly is a potent inhibitor of the fatty acid amide hydrolase (faah), the enzyme primarily responsible for the degradation of the endocannabinoid n-arachidonoyl-ethanolamine (anandamide), and was shown recently to elevate the blood levels of the this analgesic compound. 2004-04-19 2023-08-12 mouse
Benjamin F Cravatt, Aron H Lichtma. Fatty acid amide hydrolase: an emerging therapeutic target in the endocannabinoid system. Current opinion in chemical biology. vol 7. issue 4. 2004-04-07. PMID:12941421. fatty acid amide hydrolase: an emerging therapeutic target in the endocannabinoid system. 2004-04-07 2023-08-12 Not clear
Benjamin F Cravatt, Aron H Lichtma. Fatty acid amide hydrolase: an emerging therapeutic target in the endocannabinoid system. Current opinion in chemical biology. vol 7. issue 4. 2004-04-07. PMID:12941421. the recent discoveries of anandamide, a natural lipid ligand for cb1, and an enzyme, fatty acid amide hydrolase (faah), that terminates anandamide signaling have inspired pharmacological strategies to augment endogenous cannabinoid ('endocannabinoid') activity with faah inhibitors, which might exhibit superior selectivity in their elicited behavioral effects compared with direct cb1 agonists. 2004-04-07 2023-08-12 Not clear
Vincenzo Di Marz. Manipulation of the endocannabinoid system by a general anaesthetic. British journal of pharmacology. vol 139. issue 5. 2004-03-09. PMID:12839861. an article appearing in this issue of the british journal of pharmacology shows for the first time that the general anaesthetic propofol inhibits one of the enzymes catalysing endocannabinoid hydrolysis and inactivation, the fatty acid amide hydrolase, thereby enhancing the brain levels of anandamide and 2-arachidonoylglycerol in mouse brain. 2004-03-09 2023-08-12 mouse
Sachin Patel, Eric R Wohlfeil, David J Rademacher, Erica J Carrier, LaToya J Perry, Abhijit Kundu, J R Falck, Kasem Nithipatikom, William B Campbell, Cecilia J Hillar. The general anesthetic propofol increases brain N-arachidonylethanolamine (anandamide) content and inhibits fatty acid amide hydrolase. British journal of pharmacology. vol 139. issue 5. 2004-03-09. PMID:12839875. these data suggest that propofol activation of the endocannabinoid system, possibly via inhibition of anandamide catabolism, contributes to the sedative properties of propofol and that faah could be a novel target for anesthetic development. 2004-03-09 2023-08-12 mouse
Siham El Fangour, Laurence Balas, Jean-Claude Rossi, Andrey Fedenyuk, Natalia Gretskaya, Mikhail Bobrov, Vladimir Bezuglov, Cecilia J Hillard, Thierry Duran. Hemisynthesis and preliminary evaluation of novel endocannabinoid analogues. Bioorganic & medicinal chemistry letters. vol 13. issue 12. 2004-02-11. PMID:12781177. three new endocannabinoid analogues in which amide moiety was replaced either by oxomethylene group or ester moiety with simultaneous substitution of both alpha-hydrogens with methyl groups were synthesized and their abilities to interact with cb1-receptor and faah were investigated. 2004-02-11 2023-08-12 Not clear