Global InformationAnandamide information
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| Preferred IUPAC name
(5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)icosa-5,8,11,14-tetraenamide | |
| Other names
N-arachidonoylethanolamine
arachidonoylethanolamide | |
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| MeSH | Anandamide |
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| Properties | |
Chemical formula
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C22H37NO2 |
| Molar mass | 347.53 g/mol |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Infobox references
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Anandamide (ANA), also known as N-arachidonoylethanolamine (AEA), an N-acylethanolamine (NAE), is a fatty acid neurotransmitter. Anandamide was the first endocannabinoid to be discovered: it participates in the body's endocannabinoid system by binding to cannabinoid receptors, the same receptors that the psychoactive compound THC in cannabis acts on. Anandamide is found in nearly all tissues in a wide range of animals.[1][2] Anandamide has also been found in plants, including small amounts in chocolate.[3] The name 'anandamide' is taken from the Sanskrit word ananda, which means "joy, bliss, delight", plus amide.[1][4]
Anandamide is derived from the non-oxidative metabolism of arachidonic acid, an essential omega-6 fatty acid. It is synthesized from N-arachidonoyl phosphatidylethanolamine by multiple pathways.[5] It is degraded primarily by the fatty acid amide hydrolase (FAAH) enzyme, which converts anandamide into ethanolamine and arachidonic acid. As such, inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.[6][7]
Anandamide is also being explored for its role in diabetic neuropathy/neuropathy, as cannabinoids as well as exogenous or endogenous anandamide, demonstrate broad-spectrum antinociceptive properties in a model of painful diabetic neuropathy, mediated through peripheral activation of both cannabinoid receptors, i.e. CB1 and CB2,[8][9] beside involvement of transient receptor vanilloid type-1 (TRPV1) channels in the pain modulation, as endovanilloid signalling modulates local pain,[10] as well as in reduction of inflammation associated with renal injury.[11]
- ^ a b Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, et al. (December 1992). "Isolation and structure of a brain constituent that binds to the cannabinoid receptor". Science. 258 (5090): 1946–1949. Bibcode:1992Sci...258.1946D. doi:10.1126/science.1470919. PMID 1470919.
- ^ Martin BR, Mechoulam R, Razdan RK (1999). "Discovery and characterization of endogenous cannabinoids". Life Sciences. 65 (6–7): 573–595. doi:10.1016/S0024-3205(99)00281-7. PMID 10462059.
- ^ di Tomaso E, Beltramo M, Piomelli D (August 1996). "Brain cannabinoids in chocolate". Nature (Submitted manuscript). 382 (6593): 677–678. Bibcode:1996Natur.382..677D. doi:10.1038/382677a0. PMID 8751435. S2CID 4325706.
- ^ Mechoulam R, Fride E (1995). "The unpaved road to the endogenous brain cannabinoid ligands, the anandamides". In Pertwee RG (ed.). Cannabinoid receptors. Boston: Academic Press. pp. 233–258. ISBN 978-0-12-551460-6.
- ^ Wang J, Ueda N (September 2009). "Biology of endocannabinoid synthesis system". Prostaglandins & Other Lipid Mediators. 89 (3–4): 112–119. doi:10.1016/j.prostaglandins.2008.12.002. PMID 19126434.
- ^ Gaetani S, Dipasquale P, Romano A, Righetti L, Cassano T, Piomelli D, Cuomo V (2009). "The endocannabinoid system as a target for novel anxiolytic and antidepressant drugs". International Review of Neurobiology. 85: 57–72. doi:10.1016/S0074-7742(09)85005-8. ISBN 9780123748935. PMID 19607961.
- ^ Hwang J, Adamson C, Butler D, Janero DR, Makriyannis A, Bahr BA (April 2010). "Enhancement of endocannabinoid signaling by fatty acid amide hydrolase inhibition: a neuroprotective therapeutic modality". Life Sciences. 86 (15–16): 615–623. doi:10.1016/j.lfs.2009.06.003. PMC 2848893. PMID 19527737.
- ^ Schreiber, Anne K.; Neufeld, Manuele; Jesus, Carlos H. A.; Cunha, Joice M. (2012-12-01). "Peripheral antinociceptive effect of anandamide and drugs that affect the endocannabinoid system on the formalin test in normal and streptozotocin-diabetic rats". Neuropharmacology. 63 (8): 1286–1297. doi:10.1016/j.neuropharm.2012.08.009. ISSN 0028-3908. PMID 22959964. S2CID 801794.
- ^ Ellington, Heather C; Cotter, Mary A; Cameron, Norman E; Ross, Ruth A (2002-06-01). "The effect of cannabinoids on capsaicin-evoked calcitonin gene-related peptide (CGRP) release from the isolated paw skin of diabetic and non-diabetic rats". Neuropharmacology. 42 (7): 966–975. doi:10.1016/S0028-3908(02)00040-0. ISSN 0028-3908. PMID 12069907. S2CID 29219641.
- ^ Silva, M.; Martins, D.; Charrua, A.; Piscitelli, F.; Tavares, I.; Morgado, C.; Di Marzo, V. (2016-08-01). "Endovanilloid control of pain modulation by the rostroventromedial medulla in an animal model of diabetic neuropathy". Neuropharmacology. 107: 49–57. doi:10.1016/j.neuropharm.2016.03.007. ISSN 0028-3908. PMID 26965218. S2CID 24034722.
- ^ Schreiber, Anne K.; Neufeld, Manuele; Jesus, Carlos H. A.; Cunha, Joice M. (2012-12-01). "Peripheral antinociceptive effect of anandamide and drugs that affect the endocannabinoid system on the formalin test in normal and streptozotocin-diabetic rats". Neuropharmacology. 63 (8): 1286–1297. doi:10.1016/j.neuropharm.2012.08.009. ISSN 0028-3908. PMID 22959964. S2CID 801794.