Cannabis Ruderalis

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'''''N''-Arachidonoyl dopamine''' ('''NADA''') is an [[endocannabinoid]] that acts as an [[agonist]] of the [[Cannabinoid receptor type 1|CB<sub>1</sub> receptor]]<nowiki/>and the [[TRPV1|transient receptor potential V1]] (TRPV1) [[ion channel]]. NADA was first described as a putative endocannabinoid (agonist for the CB<sub>1</sub> receptor) in 2000<ref name=":0">{{Cite journal|title = N-acyl-dopamines: novel synthetic CB(1) cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo|url = http://www.ncbi.nlm.nih.gov/pubmed/11042139|journal = The Biochemical Journal|date = 2000-11-01|issn = 0264-6021|pmc = 1221424|pmid = 11042139|pages = 817-824|volume = 351 Pt 3|first = T.|last = Bisogno|first2 = D.|last2 = Melck|first3 = null|last3 = Bobrov MYu|first4 = N. M.|last4 = Gretskaya|first5 = V. V.|last5 = Bezuglov|first6 = L.|last6 = De Petrocellis|first7 = V.|last7 = Di Marzo}}</ref> and was subsequently identified as an endovanilloid (agonist for TRPV1) in 2002<ref name=":1">{{Cite journal|title = An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=12060783|journal = Proceedings of the National Academy of Sciences of the United States of America|date = 2002-06-11|issn = 0027-8424|pmc = 123079|pmid = 12060783|pages = 8400-8405|volume = 99|issue = 12|doi = 10.1073/pnas.122196999|first = Susan M.|last = Huang|first2 = Tiziana|last2 = Bisogno|first3 = Marcello|last3 = Trevisani|first4 = Abdulmonem|last4 = Al-Hayani|first5 = Luciano|last5 = De Petrocellis|first6 = Filomena|last6 = Fezza|first7 = Michele|last7 = Tognetto|first8 = Timothy J.|last8 = Petros|first9 = Jocelyn F.|last9 = Krey}}</ref>. NADA is an endogenous arachidonic acid based lipid found in the brain of rats, with especially high concentrations in the [[hippocampus]], [[cerebellum]], and [[striatum]]<ref name=":1" />. It activates the TRPV1 channel with an [[EC50|EC<sub>50</sub>]] of approximately of 50nM. The high potency makes it the putative [[endogenous]] TRPV1 agonist.<ref name="pmid12060783">{{ cite journal | author = Huang SM, Bisogno T, Trevisani M, Al-Hayani A, De Petrocellis L, Fezza F, Tognetto M, Petros TJ, Krey JF, Chu CJ, Miller JD, Davies SN, Geppetti P, Walker JM, Di Marzo V | title = An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors | journal = Proceedings of the National Academy of Sciences of the United States of America |date=June 2002 | volume = 99 | issue = 12 | pages = 8400–5 | pmid = 12060783 | pmc = 123079 | doi = 10.1073/pnas.122196999 }}</ref>
'''''N''-Arachidonoyl dopamine''' ('''NADA''') is an [[endocannabinoid]] that acts as an [[agonist]] of the [[Cannabinoid receptor type 1|CB<sub>1</sub> receptor]] <nowiki/>and the [[TRPV1|transient receptor potential V1]] (TRPV1) [[ion channel]]. NADA was first described as a putative endocannabinoid (agonist for the CB<sub>1</sub> receptor) in 2000<ref name=":0">{{Cite journal|title = N-acyl-dopamines: novel synthetic CB(1) cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo|url = http://www.ncbi.nlm.nih.gov/pubmed/11042139|journal = The Biochemical Journal|date = 2000-11-01|issn = 0264-6021|pmc = 1221424|pmid = 11042139|pages = 817-824|volume = 351 Pt 3|first = T.|last = Bisogno|first2 = D.|last2 = Melck|first3 = null|last3 = Bobrov MYu|first4 = N. M.|last4 = Gretskaya|first5 = V. V.|last5 = Bezuglov|first6 = L.|last6 = De Petrocellis|first7 = V.|last7 = Di Marzo}}</ref> and was subsequently identified as an endovanilloid (agonist for TRPV1) in 2002<ref name=":1">{{Cite journal|title = An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=12060783|journal = Proceedings of the National Academy of Sciences of the United States of America|date = 2002-06-11|issn = 0027-8424|pmc = 123079|pmid = 12060783|pages = 8400-8405|volume = 99|issue = 12|doi = 10.1073/pnas.122196999|first = Susan M.|last = Huang|first2 = Tiziana|last2 = Bisogno|first3 = Marcello|last3 = Trevisani|first4 = Abdulmonem|last4 = Al-Hayani|first5 = Luciano|last5 = De Petrocellis|first6 = Filomena|last6 = Fezza|first7 = Michele|last7 = Tognetto|first8 = Timothy J.|last8 = Petros|first9 = Jocelyn F.|last9 = Krey}}</ref>. NADA is an endogenous arachidonic acid based lipid found in the brain of rats, with especially high concentrations in the [[hippocampus]], [[cerebellum]], and [[striatum]]<ref name=":1" />. It activates the TRPV1 channel with an [[EC50|EC<sub>50</sub>]] of approximately of 50nM. The high potency makes it the putative [[endogenous]] TRPV1 agonist.<ref name="pmid12060783">{{ cite journal | author = Huang SM, Bisogno T, Trevisani M, Al-Hayani A, De Petrocellis L, Fezza F, Tognetto M, Petros TJ, Krey JF, Chu CJ, Miller JD, Davies SN, Geppetti P, Walker JM, Di Marzo V | title = An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors | journal = Proceedings of the National Academy of Sciences of the United States of America |date=June 2002 | volume = 99 | issue = 12 | pages = 8400–5 | pmid = 12060783 | pmc = 123079 | doi = 10.1073/pnas.122196999 }}</ref>


In mice, NADA was shown to induce the tetrad of physiological paradigms associated with cannabinoids: hypothermia, hypo-locomotion, catalepsy, and analgesia<ref name=":0" /><ref>{{Cite journal|title = Synthesis and biological evaluation of novel amides of polyunsaturated fatty acids with dopamine|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=11229744|journal = Bioorganic & Medicinal Chemistry Letters|date = 2001-02-26|issn = 0960-894X|pmid = 11229744|pages = 447-449|volume = 11|issue = 4|first = V.|last = Bezuglov|first2 = M.|last2 = Bobrov|first3 = N.|last3 = Gretskaya|first4 = A.|last4 = Gonchar|first5 = G.|last5 = Zinchenko|first6 = D.|last6 = Melck|first7 = T.|last7 = Bisogno|first8 = V.|last8 = Di Marzo|first9 = D.|last9 = Kuklev}}</ref><ref>{{Cite journal|title = Pharmacology and stereoselectivity of structurally novel cannabinoids in mice|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=2849657|journal = The Journal of Pharmacology and Experimental Therapeutics|date = 1988-12-01|issn = 0022-3565|pmid = 2849657|pages = 1046-1051|volume = 247|issue = 3|first = P. J.|last = Little|first2 = D. R.|last2 = Compton|first3 = M. R.|last3 = Johnson|first4 = L. S.|last4 = Melvin|first5 = B. R.|last5 = Martin}}</ref>. NADA has been found to play a regulatory role in both the peripheral and central nervous systems, and displays antioxidant and neuroprotectant properties<ref>{{Cite journal|title = An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=12060783|journal = Proceedings of the National Academy of Sciences of the United States of America|date = 2002-06-11|issn = 0027-8424|pmc = 123079|pmid = 12060783|pages = 8400-8405|volume = 99|issue = 12|doi = 10.1073/pnas.122196999|first = Susan M.|last = Huang|first2 = Tiziana|last2 = Bisogno|first3 = Marcello|last3 = Trevisani|first4 = Abdulmonem|last4 = Al-Hayani|first5 = Luciano|last5 = De Petrocellis|first6 = Filomena|last6 = Fezza|first7 = Michele|last7 = Tognetto|first8 = Timothy J.|last8 = Petros|first9 = Jocelyn F.|last9 = Krey}}</ref><ref>{{Cite journal|title = Modulation of trigeminal sensory neuron activity by the dual cannabinoid-vanilloid agonists anandamide, N-arachidonoyl-dopamine and arachidonyl-2-chloroethylamide|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=15006899|journal = British Journal of Pharmacology|date = 2004-04-01|issn = 0007-1188|pmc = 1574881|pmid = 15006899|pages = 1118-1130|volume = 141|issue = 7|doi = 10.1038/sj.bjp.0705711|first = Theodore J.|last = Price|first2 = Amol|last2 = Patwardhan|first3 = Armen N.|last3 = Akopian|first4 = Kenneth M.|last4 = Hargreaves|first5 = Christopher M.|last5 = Flores}}</ref><ref>{{Cite journal|title = Modulation of trigeminal sensory neuron activity by the dual cannabinoid-vanilloid agonists anandamide, N-arachidonoyl-dopamine and arachidonyl-2-chloroethylamide|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=15006899|journal = British Journal of Pharmacology|date = 2004-04-01|issn = 0007-1188|pmc = 1574881|pmid = 15006899|pages = 1118-1130|volume = 141|issue = 7|doi = 10.1038/sj.bjp.0705711|first = Theodore J.|last = Price|first2 = Amol|last2 = Patwardhan|first3 = Armen N.|last3 = Akopian|first4 = Kenneth M.|last4 = Hargreaves|first5 = Christopher M.|last5 = Flores}}</ref><ref>{{Cite journal|title = N-arachidonoyl-dopamine tunes synaptic transmission onto dopaminergic neurons by activating both cannabinoid and vanilloid receptors|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=16760924|journal = Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology|date = 2007-02-01|issn = 0893-133X|pmid = 16760924|pages = 298-308|volume = 32|issue = 2|doi = 10.1038/sj.npp.1301118|first = Silvia|last = Marinelli|first2 = Vincenzo|last2 = Di Marzo|first3 = Fulvio|last3 = Florenzano|first4 = Filomena|last4 = Fezza|first5 = Maria Teresa|last5 = Viscomi|first6 = Mario|last6 = van der Stelt|first7 = Giorgio|last7 = Bernardi|first8 = Marco|last8 = Molinari|first9 = Mauro|last9 = Maccarrone}}</ref><ref>{{Cite journal|title = TRPV1 and CB(1) receptor-mediated effects of the endovanilloid/endocannabinoid N-arachidonoyl-dopamine on primary afferent fibre and spinal cord neuronal responses in the rat|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=15245490|journal = The European Journal of Neuroscience|date = 2004-07-01|issn = 0953-816X|pmid = 15245490|pages = 175-184|volume = 20|issue = 1|doi = 10.1111/j.1460-9568.2004.03481.x|first = Devi R.|last = Sagar|first2 = Paul A.|last2 = Smith|first3 = Paul J.|last3 = Millns|first4 = Darren|last4 = Smart|first5 = David A.|last5 = Kendall|first6 = Victoria|last6 = Chapman}}</ref>. NADA has also been implicated in smooth muscle contraction and vasorelaxation in blood vessels<ref>{{Cite journal|title = Antioxidant and neuroprotective properties of N-arachidonoyldopamine|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=18069125|journal = Neuroscience Letters|date = 2008-01-24|issn = 0304-3940|pmid = 18069125|pages = 6-11|volume = 431|issue = 1|doi = 10.1016/j.neulet.2007.11.010|first = Mikhail Yu|last = Bobrov|first2 = Anatoly A.|last2 = Lizhin|first3 = Ekaterina L.|last3 = Andrianova|first4 = Natalia M.|last4 = Gretskaya|first5 = Lidia E.|last5 = Frumkina|first6 = Leonid G.|last6 = Khaspekov|first7 = Vladimir V.|last7 = Bezuglov}}</ref><ref>{{Cite journal|title = Capsaicin-like effects of N-arachidonoyl-dopamine in the isolated guinea pig bronchi and urinary bladder|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=12954366|journal = European Journal of Pharmacology|date = 2003-08-15|issn = 0014-2999|pmid = 12954366|pages = 107-114|volume = 475|issue = 1-3|first = Selena|last = Harrison|first2 = Luciano|last2 = De Petrocellis|first3 = Marcello|last3 = Trevisani|first4 = Francesca|last4 = Benvenuti|first5 = Maurizio|last5 = Bifulco|first6 = Pierangelo|last6 = Geppetti|first7 = Vincenzo|last7 = Di Marzo}}</ref><ref>{{Cite journal|title = Characterisation of the vasorelaxant properties of the novel endocannabinoid N-arachidonoyl-dopamine (NADA)|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=14769783|journal = British Journal of Pharmacology|date = 2004-03-01|issn = 0007-1188|pmc = 1574254|pmid = 14769783|pages = 803-812|volume = 141|issue = 5|doi = 10.1038/sj.bjp.0705643|first = Saoirse E.|last = O'Sullivan|first2 = David A.|last2 = Kendall|first3 = Michael D.|last3 = Randall}}</ref><ref>{{Cite journal|title = Time-dependent vascular effects of Endocannabinoids mediated by peroxisome proliferator-activated receptor gamma (PPARγ)|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=19421417|journal = PPAR research|date = 2009-01-01|issn = 1687-4757|pmc = 2676321|pmid = 19421417|pages = 425289|volume = 2009|doi = 10.1155/2009/425289|first = Saoirse E.|last = O'Sullivan|first2 = David A.|last2 = Kendall|first3 = Michael D.|last3 = Randall}}</ref>. Additionally, NADA has been observed to suppress inflammatory activation of human Jurkat T cells and to inhibit the release of prostaglandin E2 (PGE2) from LPS-activated astrocytes, microglia and mouse brain ECs (MEC-Brain)<ref>{{Cite journal|title = Opposite effects of anandamide and N-arachidonoyl dopamine in the regulation of prostaglandin E and 8-iso-PGF formation in primary glial cells|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=19200337|journal = Journal of Neurochemistry|date = 2009-04-01|issn = 1471-4159|pmid = 19200337|pages = 452-464|volume = 109|issue = 2|doi = 10.1111/j.1471-4159.2009.05966.x|first = Carmen M.|last = Navarrete|first2 = Bernd L.|last2 = Fiebich|first3 = Amaya García|last3 = de Vinuesa|first4 = Sandra|last4 = Hess|first5 = Antonio C. P.|last5 = de Oliveira|first6 = Eduardo|last6 = Candelario-Jalil|first7 = Francisco J.|last7 = Caballero|first8 = Marco A.|last8 = Calzado|first9 = Eduardo|last9 = Muñoz}}</ref><ref>{{Cite journal|title = Endogenous N-acyl-dopamines induce COX-2 expression in brain endothelial cells by stabilizing mRNA through a p38 dependent pathway|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=20206142|journal = Biochemical Pharmacology|date = 2010-06-15|issn = 1873-2968|pmid = 20206142|pages = 1805-1814|volume = 79|issue = 12|doi = 10.1016/j.bcp.2010.02.014|first = Carmen M.|last = Navarrete|first2 = Moisés|last2 = Pérez|first3 = Amaya García|last3 = de Vinuesa|first4 = Juan A.|last4 = Collado|first5 = Bernd L.|last5 = Fiebich|first6 = Marco A.|last6 = Calzado|first7 = Eduardo|last7 = Muñoz}}</ref><ref>{{Cite journal|title = Immunosuppressive activity of endovanilloids: N-arachidonoyl-dopamine inhibits activation of the NF-kappa B, NFAT, and activator protein 1 signaling pathways|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=14764703|journal = Journal of Immunology (Baltimore, Md.: 1950)|date = 2004-02-15|issn = 0022-1767|pmid = 14764703|pages = 2341-2351|volume = 172|issue = 4|first = Rocío|last = Sancho|first2 = Antonio|last2 = Macho|first3 = Laureano|last3 = de La Vega|first4 = Marco A.|last4 = Calzado|first5 = Bernd L.|last5 = Fiebich|first6 = Giovanni|last6 = Appendino|first7 = Eduardo|last7 = Muñoz}}</ref>. NADA also promotes the inflammatory resolution of human endothelial cells activated by both endogenous (''i.e.'' TNF) and exogenous (''i.e.'' bacterial derived lipopolysaccharide (TLR4 agonist) and FSL-1 (TLR2/6 agonist)) inflammatory mediators<ref>{{Cite journal|title = The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=24644287|journal = The Journal of Biological Chemistry|date = 2014-05-09|issn = 1083-351X|pmc = 4036321|pmid = 24644287|pages = 13079-13100|volume = 289|issue = 19|doi = 10.1074/jbc.M113.536953|first = Kevin|last = Wilhelmsen|first2 = Samira|last2 = Khakpour|first3 = Alphonso|last3 = Tran|first4 = Kayla|last4 = Sheehan|first5 = Mark|last5 = Schumacher|first6 = Fengyun|last6 = Xu|first7 = Judith|last7 = Hellman}}</ref>. Furthermore, NADA also displays inhibitory activity in HIV-1 replication assays<ref>{{Cite journal|title = Mechanisms of HIV-1 inhibition by the lipid mediator N-arachidonoyldopamine|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=16148147|journal = Journal of Immunology (Baltimore, Md.: 1950)|date = 2005-09-15|issn = 0022-1767|pmid = 16148147|pages = 3990-3999|volume = 175|issue = 6|first = Rocío|last = Sancho|first2 = Laureano|last2 = de la Vega|first3 = Antonio|last3 = Macho|first4 = Giovanni|last4 = Appendino|first5 = Vincenzo|last5 = Di Marzo|first6 = Eduardo|last6 = Muñoz}}</ref>. Finally, NADA can prevent the degranulation and release of TNF from RBL- 2H3 mast cells treated with an IgE-antigen complex<ref>{{Cite journal|title = Inhibitory effect of N-Acyl dopamines on IgE-mediated allergic response in RBL-2H3 cells|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=23377981|journal = Lipids|date = 2013-04-01|issn = 1558-9307|pmid = 23377981|pages = 383-393|volume = 48|issue = 4|doi = 10.1007/s11745-013-3758-6|first = Jae-Myung|last = Yoo|first2 = Eun Seok|last2 = Park|first3 = Mee Ree|last3 = Kim|first4 = Dai-Eun|last4 = Sok}}</ref>. Together, theses studies show that physiological functions attributed to NADA are multifaceted, and include the potential to modulate the immune response.
In mice, NADA was shown to induce the tetrad of physiological paradigms associated with cannabinoids: hypothermia, hypo-locomotion, catalepsy, and analgesia<ref name=":0" /><ref>{{Cite journal|title = Synthesis and biological evaluation of novel amides of polyunsaturated fatty acids with dopamine|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=11229744|journal = Bioorganic & Medicinal Chemistry Letters|date = 2001-02-26|issn = 0960-894X|pmid = 11229744|pages = 447-449|volume = 11|issue = 4|first = V.|last = Bezuglov|first2 = M.|last2 = Bobrov|first3 = N.|last3 = Gretskaya|first4 = A.|last4 = Gonchar|first5 = G.|last5 = Zinchenko|first6 = D.|last6 = Melck|first7 = T.|last7 = Bisogno|first8 = V.|last8 = Di Marzo|first9 = D.|last9 = Kuklev}}</ref><ref>{{Cite journal|title = Pharmacology and stereoselectivity of structurally novel cannabinoids in mice|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=2849657|journal = The Journal of Pharmacology and Experimental Therapeutics|date = 1988-12-01|issn = 0022-3565|pmid = 2849657|pages = 1046-1051|volume = 247|issue = 3|first = P. J.|last = Little|first2 = D. R.|last2 = Compton|first3 = M. R.|last3 = Johnson|first4 = L. S.|last4 = Melvin|first5 = B. R.|last5 = Martin}}</ref>. NADA has been found to play a regulatory role in both the peripheral and central nervous systems, and displays antioxidant and neuroprotectant properties<ref>{{Cite journal|title = An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=12060783|journal = Proceedings of the National Academy of Sciences of the United States of America|date = 2002-06-11|issn = 0027-8424|pmc = 123079|pmid = 12060783|pages = 8400-8405|volume = 99|issue = 12|doi = 10.1073/pnas.122196999|first = Susan M.|last = Huang|first2 = Tiziana|last2 = Bisogno|first3 = Marcello|last3 = Trevisani|first4 = Abdulmonem|last4 = Al-Hayani|first5 = Luciano|last5 = De Petrocellis|first6 = Filomena|last6 = Fezza|first7 = Michele|last7 = Tognetto|first8 = Timothy J.|last8 = Petros|first9 = Jocelyn F.|last9 = Krey}}</ref><ref>{{Cite journal|title = Modulation of trigeminal sensory neuron activity by the dual cannabinoid-vanilloid agonists anandamide, N-arachidonoyl-dopamine and arachidonyl-2-chloroethylamide|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=15006899|journal = British Journal of Pharmacology|date = 2004-04-01|issn = 0007-1188|pmc = 1574881|pmid = 15006899|pages = 1118-1130|volume = 141|issue = 7|doi = 10.1038/sj.bjp.0705711|first = Theodore J.|last = Price|first2 = Amol|last2 = Patwardhan|first3 = Armen N.|last3 = Akopian|first4 = Kenneth M.|last4 = Hargreaves|first5 = Christopher M.|last5 = Flores}}</ref><ref>{{Cite journal|title = Modulation of trigeminal sensory neuron activity by the dual cannabinoid-vanilloid agonists anandamide, N-arachidonoyl-dopamine and arachidonyl-2-chloroethylamide|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=15006899|journal = British Journal of Pharmacology|date = 2004-04-01|issn = 0007-1188|pmc = 1574881|pmid = 15006899|pages = 1118-1130|volume = 141|issue = 7|doi = 10.1038/sj.bjp.0705711|first = Theodore J.|last = Price|first2 = Amol|last2 = Patwardhan|first3 = Armen N.|last3 = Akopian|first4 = Kenneth M.|last4 = Hargreaves|first5 = Christopher M.|last5 = Flores}}</ref><ref>{{Cite journal|title = N-arachidonoyl-dopamine tunes synaptic transmission onto dopaminergic neurons by activating both cannabinoid and vanilloid receptors|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=16760924|journal = Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology|date = 2007-02-01|issn = 0893-133X|pmid = 16760924|pages = 298-308|volume = 32|issue = 2|doi = 10.1038/sj.npp.1301118|first = Silvia|last = Marinelli|first2 = Vincenzo|last2 = Di Marzo|first3 = Fulvio|last3 = Florenzano|first4 = Filomena|last4 = Fezza|first5 = Maria Teresa|last5 = Viscomi|first6 = Mario|last6 = van der Stelt|first7 = Giorgio|last7 = Bernardi|first8 = Marco|last8 = Molinari|first9 = Mauro|last9 = Maccarrone}}</ref><ref>{{Cite journal|title = TRPV1 and CB(1) receptor-mediated effects of the endovanilloid/endocannabinoid N-arachidonoyl-dopamine on primary afferent fibre and spinal cord neuronal responses in the rat|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=15245490|journal = The European Journal of Neuroscience|date = 2004-07-01|issn = 0953-816X|pmid = 15245490|pages = 175-184|volume = 20|issue = 1|doi = 10.1111/j.1460-9568.2004.03481.x|first = Devi R.|last = Sagar|first2 = Paul A.|last2 = Smith|first3 = Paul J.|last3 = Millns|first4 = Darren|last4 = Smart|first5 = David A.|last5 = Kendall|first6 = Victoria|last6 = Chapman}}</ref>. NADA has also been implicated in smooth muscle contraction and vasorelaxation in blood vessels<ref>{{Cite journal|title = Antioxidant and neuroprotective properties of N-arachidonoyldopamine|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=18069125|journal = Neuroscience Letters|date = 2008-01-24|issn = 0304-3940|pmid = 18069125|pages = 6-11|volume = 431|issue = 1|doi = 10.1016/j.neulet.2007.11.010|first = Mikhail Yu|last = Bobrov|first2 = Anatoly A.|last2 = Lizhin|first3 = Ekaterina L.|last3 = Andrianova|first4 = Natalia M.|last4 = Gretskaya|first5 = Lidia E.|last5 = Frumkina|first6 = Leonid G.|last6 = Khaspekov|first7 = Vladimir V.|last7 = Bezuglov}}</ref><ref>{{Cite journal|title = Capsaicin-like effects of N-arachidonoyl-dopamine in the isolated guinea pig bronchi and urinary bladder|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=12954366|journal = European Journal of Pharmacology|date = 2003-08-15|issn = 0014-2999|pmid = 12954366|pages = 107-114|volume = 475|issue = 1-3|first = Selena|last = Harrison|first2 = Luciano|last2 = De Petrocellis|first3 = Marcello|last3 = Trevisani|first4 = Francesca|last4 = Benvenuti|first5 = Maurizio|last5 = Bifulco|first6 = Pierangelo|last6 = Geppetti|first7 = Vincenzo|last7 = Di Marzo}}</ref><ref>{{Cite journal|title = Characterisation of the vasorelaxant properties of the novel endocannabinoid N-arachidonoyl-dopamine (NADA)|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=14769783|journal = British Journal of Pharmacology|date = 2004-03-01|issn = 0007-1188|pmc = 1574254|pmid = 14769783|pages = 803-812|volume = 141|issue = 5|doi = 10.1038/sj.bjp.0705643|first = Saoirse E.|last = O'Sullivan|first2 = David A.|last2 = Kendall|first3 = Michael D.|last3 = Randall}}</ref><ref>{{Cite journal|title = Time-dependent vascular effects of Endocannabinoids mediated by peroxisome proliferator-activated receptor gamma (PPARγ)|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=19421417|journal = PPAR research|date = 2009-01-01|issn = 1687-4757|pmc = 2676321|pmid = 19421417|pages = 425289|volume = 2009|doi = 10.1155/2009/425289|first = Saoirse E.|last = O'Sullivan|first2 = David A.|last2 = Kendall|first3 = Michael D.|last3 = Randall}}</ref>. Additionally, NADA has been observed to suppress inflammatory activation of human Jurkat T cells and to inhibit the release of prostaglandin E2 (PGE2) from LPS-activated astrocytes, microglia and mouse brain ECs (MEC-Brain)<ref>{{Cite journal|title = Opposite effects of anandamide and N-arachidonoyl dopamine in the regulation of prostaglandin E and 8-iso-PGF formation in primary glial cells|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=19200337|journal = Journal of Neurochemistry|date = 2009-04-01|issn = 1471-4159|pmid = 19200337|pages = 452-464|volume = 109|issue = 2|doi = 10.1111/j.1471-4159.2009.05966.x|first = Carmen M.|last = Navarrete|first2 = Bernd L.|last2 = Fiebich|first3 = Amaya García|last3 = de Vinuesa|first4 = Sandra|last4 = Hess|first5 = Antonio C. P.|last5 = de Oliveira|first6 = Eduardo|last6 = Candelario-Jalil|first7 = Francisco J.|last7 = Caballero|first8 = Marco A.|last8 = Calzado|first9 = Eduardo|last9 = Muñoz}}</ref><ref>{{Cite journal|title = Endogenous N-acyl-dopamines induce COX-2 expression in brain endothelial cells by stabilizing mRNA through a p38 dependent pathway|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=20206142|journal = Biochemical Pharmacology|date = 2010-06-15|issn = 1873-2968|pmid = 20206142|pages = 1805-1814|volume = 79|issue = 12|doi = 10.1016/j.bcp.2010.02.014|first = Carmen M.|last = Navarrete|first2 = Moisés|last2 = Pérez|first3 = Amaya García|last3 = de Vinuesa|first4 = Juan A.|last4 = Collado|first5 = Bernd L.|last5 = Fiebich|first6 = Marco A.|last6 = Calzado|first7 = Eduardo|last7 = Muñoz}}</ref><ref>{{Cite journal|title = Immunosuppressive activity of endovanilloids: N-arachidonoyl-dopamine inhibits activation of the NF-kappa B, NFAT, and activator protein 1 signaling pathways|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=14764703|journal = Journal of Immunology (Baltimore, Md.: 1950)|date = 2004-02-15|issn = 0022-1767|pmid = 14764703|pages = 2341-2351|volume = 172|issue = 4|first = Rocío|last = Sancho|first2 = Antonio|last2 = Macho|first3 = Laureano|last3 = de La Vega|first4 = Marco A.|last4 = Calzado|first5 = Bernd L.|last5 = Fiebich|first6 = Giovanni|last6 = Appendino|first7 = Eduardo|last7 = Muñoz}}</ref>. NADA also promotes the inflammatory resolution of human endothelial cells activated by both endogenous (''i.e.'' TNF) and exogenous (''i.e.'' bacterial derived lipopolysaccharide (TLR4 agonist) and FSL-1 (TLR2/6 agonist)) inflammatory mediators<ref>{{Cite journal|title = The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=24644287|journal = The Journal of Biological Chemistry|date = 2014-05-09|issn = 1083-351X|pmc = 4036321|pmid = 24644287|pages = 13079-13100|volume = 289|issue = 19|doi = 10.1074/jbc.M113.536953|first = Kevin|last = Wilhelmsen|first2 = Samira|last2 = Khakpour|first3 = Alphonso|last3 = Tran|first4 = Kayla|last4 = Sheehan|first5 = Mark|last5 = Schumacher|first6 = Fengyun|last6 = Xu|first7 = Judith|last7 = Hellman}}</ref>. Furthermore, NADA also displays inhibitory activity in HIV-1 replication assays<ref>{{Cite journal|title = Mechanisms of HIV-1 inhibition by the lipid mediator N-arachidonoyldopamine|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=16148147|journal = Journal of Immunology (Baltimore, Md.: 1950)|date = 2005-09-15|issn = 0022-1767|pmid = 16148147|pages = 3990-3999|volume = 175|issue = 6|first = Rocío|last = Sancho|first2 = Laureano|last2 = de la Vega|first3 = Antonio|last3 = Macho|first4 = Giovanni|last4 = Appendino|first5 = Vincenzo|last5 = Di Marzo|first6 = Eduardo|last6 = Muñoz}}</ref>. Finally, NADA can prevent the degranulation and release of TNF from RBL- 2H3 mast cells treated with an IgE-antigen complex<ref>{{Cite journal|title = Inhibitory effect of N-Acyl dopamines on IgE-mediated allergic response in RBL-2H3 cells|url = http://www.ncbi.nlm.nih.gov/pubmed/?term=23377981|journal = Lipids|date = 2013-04-01|issn = 1558-9307|pmid = 23377981|pages = 383-393|volume = 48|issue = 4|doi = 10.1007/s11745-013-3758-6|first = Jae-Myung|last = Yoo|first2 = Eun Seok|last2 = Park|first3 = Mee Ree|last3 = Kim|first4 = Dai-Eun|last4 = Sok}}</ref>. Together, theses studies show that physiological functions attributed to NADA are multifaceted, and include the potential to modulate the immune response.

Revision as of 07:55, 9 January 2016

N-Arachidonoyl dopamine
Names
IUPAC name
(5Z,8Z,11Z,14Z)-N-[2-(3,4-dihydroxyphenyl)-ethyl]icosa-5,8,11,14-tetraenamide
Other names
NADA
Identifiers
3D model (JSmol)
ChEMBL
ChemSpider
  • InChI=1S/C28H41NO3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-28(32)29-23-22-25-20-21-26(30)27(31)24-25/h6-7,9-10,12-13,15-16,20-21,24,30-31H,2-5,8,11,14,17-19,22-23H2,1H3,(H,29,32)/b7-6-,10-9-,13-12-,16-15- checkY
    Key: MVVPIAAVGAWJNQ-DOFZRALJSA-N checkY
  • InChI=1/C28H41NO3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-28(32)29-23-22-25-20-21-26(30)27(31)24-25/h6-7,9-10,12-13,15-16,20-21,24,30-31H,2-5,8,11,14,17-19,22-23H2,1H3,(H,29,32)/b7-6-,10-9-,13-12-,16-15-
    Key: MVVPIAAVGAWJNQ-DOFZRALJBM
  • CCCCC\C=C/C\C=C/C\C=C/C\C=C/CCCC(=O)NCCC1=CC(=C(C=C1)O)O
Properties
C28H41NO3
Molar mass 439.63 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

N-Arachidonoyl dopamine (NADA) is an endocannabinoid that acts as an agonist of the CB1 receptor and the transient receptor potential V1 (TRPV1) ion channel. NADA was first described as a putative endocannabinoid (agonist for the CB1 receptor) in 2000[1] and was subsequently identified as an endovanilloid (agonist for TRPV1) in 2002[2]. NADA is an endogenous arachidonic acid based lipid found in the brain of rats, with especially high concentrations in the hippocampus, cerebellum, and striatum[2]. It activates the TRPV1 channel with an EC50 of approximately of 50nM. The high potency makes it the putative endogenous TRPV1 agonist.[3]

In mice, NADA was shown to induce the tetrad of physiological paradigms associated with cannabinoids: hypothermia, hypo-locomotion, catalepsy, and analgesia[1][4][5]. NADA has been found to play a regulatory role in both the peripheral and central nervous systems, and displays antioxidant and neuroprotectant properties[6][7][8][9][10]. NADA has also been implicated in smooth muscle contraction and vasorelaxation in blood vessels[11][12][13][14]. Additionally, NADA has been observed to suppress inflammatory activation of human Jurkat T cells and to inhibit the release of prostaglandin E2 (PGE2) from LPS-activated astrocytes, microglia and mouse brain ECs (MEC-Brain)[15][16][17]. NADA also promotes the inflammatory resolution of human endothelial cells activated by both endogenous (i.e. TNF) and exogenous (i.e. bacterial derived lipopolysaccharide (TLR4 agonist) and FSL-1 (TLR2/6 agonist)) inflammatory mediators[18]. Furthermore, NADA also displays inhibitory activity in HIV-1 replication assays[19]. Finally, NADA can prevent the degranulation and release of TNF from RBL- 2H3 mast cells treated with an IgE-antigen complex[20]. Together, theses studies show that physiological functions attributed to NADA are multifaceted, and include the potential to modulate the immune response.

Several cytochrome P450 endoplasmic reticulum-bound enzymes, i.e. CYP4A11, CYP4F2, CYP4F3, CYP4Z1, and CYP2U1 in humans,[21][22][23][24][25][26] Cyp4a12a and Cyp4a12b ins mice,[27] and Cyp4a1, Cyp4a2, Cyp4a3, and Cyp4a8 in rats[21] ω-hydroxylate arachidonic acid to form 20-hydroxyeicosatetraenoic acid (20-HETE) and lesser amounts of 19-hydroxyeicosatetraenoate (19-HETE) (see 20-Hydroxyeicosatetraenoic acid). Rat liver endoplasmic reticulum (i.e. microsome) preparations hydroxylated MADA to 20-hydroxy and lesser amounts of 19-hydroxy arachidonoyl dopamine products; both metabolites as well as 18-hydroxy arachidonoyl dopamine stimulated recombinant human TRPV(1) receptors, being about 10-fold less potent than NADA in doing so.[28] These results identify a variety of metabolically modified NADA's as potential TRPV1 agonists and suggest that one or more of the cited cytochrome P450 enzymes may be involved in inactivating NADA.

See also

References

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  2. ^ a b Huang, Susan M.; Bisogno, Tiziana; Trevisani, Marcello; Al-Hayani, Abdulmonem; De Petrocellis, Luciano; Fezza, Filomena; Tognetto, Michele; Petros, Timothy J.; Krey, Jocelyn F. (2002-06-11). "An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors". Proceedings of the National Academy of Sciences of the United States of America. 99 (12): 8400–8405. doi:10.1073/pnas.122196999. ISSN 0027-8424. PMC 123079. PMID 12060783.
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  4. ^ Bezuglov, V.; Bobrov, M.; Gretskaya, N.; Gonchar, A.; Zinchenko, G.; Melck, D.; Bisogno, T.; Di Marzo, V.; Kuklev, D. (2001-02-26). "Synthesis and biological evaluation of novel amides of polyunsaturated fatty acids with dopamine". Bioorganic & Medicinal Chemistry Letters. 11 (4): 447–449. ISSN 0960-894X. PMID 11229744.
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  6. ^ Huang, Susan M.; Bisogno, Tiziana; Trevisani, Marcello; Al-Hayani, Abdulmonem; De Petrocellis, Luciano; Fezza, Filomena; Tognetto, Michele; Petros, Timothy J.; Krey, Jocelyn F. (2002-06-11). "An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors". Proceedings of the National Academy of Sciences of the United States of America. 99 (12): 8400–8405. doi:10.1073/pnas.122196999. ISSN 0027-8424. PMC 123079. PMID 12060783.
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  10. ^ Sagar, Devi R.; Smith, Paul A.; Millns, Paul J.; Smart, Darren; Kendall, David A.; Chapman, Victoria (2004-07-01). "TRPV1 and CB(1) receptor-mediated effects of the endovanilloid/endocannabinoid N-arachidonoyl-dopamine on primary afferent fibre and spinal cord neuronal responses in the rat". The European Journal of Neuroscience. 20 (1): 175–184. doi:10.1111/j.1460-9568.2004.03481.x. ISSN 0953-816X. PMID 15245490.
  11. ^ Bobrov, Mikhail Yu; Lizhin, Anatoly A.; Andrianova, Ekaterina L.; Gretskaya, Natalia M.; Frumkina, Lidia E.; Khaspekov, Leonid G.; Bezuglov, Vladimir V. (2008-01-24). "Antioxidant and neuroprotective properties of N-arachidonoyldopamine". Neuroscience Letters. 431 (1): 6–11. doi:10.1016/j.neulet.2007.11.010. ISSN 0304-3940. PMID 18069125.
  12. ^ Harrison, Selena; De Petrocellis, Luciano; Trevisani, Marcello; Benvenuti, Francesca; Bifulco, Maurizio; Geppetti, Pierangelo; Di Marzo, Vincenzo (2003-08-15). "Capsaicin-like effects of N-arachidonoyl-dopamine in the isolated guinea pig bronchi and urinary bladder". European Journal of Pharmacology. 475 (1–3): 107–114. ISSN 0014-2999. PMID 12954366.
  13. ^ O'Sullivan, Saoirse E.; Kendall, David A.; Randall, Michael D. (2004-03-01). "Characterisation of the vasorelaxant properties of the novel endocannabinoid N-arachidonoyl-dopamine (NADA)". British Journal of Pharmacology. 141 (5): 803–812. doi:10.1038/sj.bjp.0705643. ISSN 0007-1188. PMC 1574254. PMID 14769783.
  14. ^ O'Sullivan, Saoirse E.; Kendall, David A.; Randall, Michael D. (2009-01-01). "Time-dependent vascular effects of Endocannabinoids mediated by peroxisome proliferator-activated receptor gamma (PPARγ)". PPAR research. 2009: 425289. doi:10.1155/2009/425289. ISSN 1687-4757. PMC 2676321. PMID 19421417.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  15. ^ Navarrete, Carmen M.; Fiebich, Bernd L.; de Vinuesa, Amaya García; Hess, Sandra; de Oliveira, Antonio C. P.; Candelario-Jalil, Eduardo; Caballero, Francisco J.; Calzado, Marco A.; Muñoz, Eduardo (2009-04-01). "Opposite effects of anandamide and N-arachidonoyl dopamine in the regulation of prostaglandin E and 8-iso-PGF formation in primary glial cells". Journal of Neurochemistry. 109 (2): 452–464. doi:10.1111/j.1471-4159.2009.05966.x. ISSN 1471-4159. PMID 19200337.
  16. ^ Navarrete, Carmen M.; Pérez, Moisés; de Vinuesa, Amaya García; Collado, Juan A.; Fiebich, Bernd L.; Calzado, Marco A.; Muñoz, Eduardo (2010-06-15). "Endogenous N-acyl-dopamines induce COX-2 expression in brain endothelial cells by stabilizing mRNA through a p38 dependent pathway". Biochemical Pharmacology. 79 (12): 1805–1814. doi:10.1016/j.bcp.2010.02.014. ISSN 1873-2968. PMID 20206142.
  17. ^ Sancho, Rocío; Macho, Antonio; de La Vega, Laureano; Calzado, Marco A.; Fiebich, Bernd L.; Appendino, Giovanni; Muñoz, Eduardo (2004-02-15). "Immunosuppressive activity of endovanilloids: N-arachidonoyl-dopamine inhibits activation of the NF-kappa B, NFAT, and activator protein 1 signaling pathways". Journal of Immunology (Baltimore, Md.: 1950). 172 (4): 2341–2351. ISSN 0022-1767. PMID 14764703.
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  19. ^ Sancho, Rocío; de la Vega, Laureano; Macho, Antonio; Appendino, Giovanni; Di Marzo, Vincenzo; Muñoz, Eduardo (2005-09-15). "Mechanisms of HIV-1 inhibition by the lipid mediator N-arachidonoyldopamine". Journal of Immunology (Baltimore, Md.: 1950). 175 (6): 3990–3999. ISSN 0022-1767. PMID 16148147.
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External links

source: https://en.wikipedia.org/w/index.php?title=N-Arachidonoyl_dopamine&diff=prev&oldid=698952297

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