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14707029

Source:http://linkedlifedata.com/resource/pubmed/id/14707029

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pubmed-article:14707029pubmed:abstractText1. The ability of the endogenous fatty acid amide, cis-oleamide (ODA), to bind to and activate cannabinoid CB(1) and CB(2) receptors was investigated. 2. ODA competitively inhibited binding of the nonselective cannabinoid agonist [(3)H]CP55,940 and the selective CB(1) antagonist [(3)H]SR141716A to rat whole-brain membranes with K(i) values of 1.14 microm (0.52-2.53 microm, Hill slope=0.80, n=6) and 2.63 microm (0.62-11.20 microm, Hill slope=0.92, n=4), respectively. AEA inhibited [(3)H]CP55,940 binding in rat whole-brain membranes with a K(i) of 428 nm (346-510 nm, Hill slope=-1.33, n=3). 3. ODA competitively inhibited [(3)H]CP55,940 binding in human CB(1) (hCB(1)) cell membranes with a K(i) value of 8.13 microm (4.97-13.32 microm, n=2). In human CB(2) transfected (hCB(2)) HEK-293T cell membranes, 100 microm ODA produced only a partial (42.5+/-7%) inhibition of [(3)H]CP55,940 binding. 4. ODA stimulated [(35)S]GTPgammaS binding in a concentration-dependent manner (EC(50)=1.64 microm (0.29-9.32 microm), R(2)=0.99, n=4-9), with maximal stimulation of 188+/-9% of basal at 100 microm. AEA stimulated [(35)S]GTPgammaS binding with an EC(50) of 10.43 microm (4.45-24.42 microm, R(2)=1.00, n=3, 195+/-4% of basal at 300 microm). Trans-oleamide (trans-ODA) failed to significantly stimulate [(35)S]GTPgammaS binding at concentrations up to 100 microm. 5. ODA (10 microm)-stimulated [(35)S]GTPgammaS binding was reversed by the selective CB(1) antagonist SR141716A (IC(50)=2.11 nm (0.32-13.77 nm), R(2)=1.00, n=6). 6. The anatomical distribution of ODA-stimulated [(35)S]GTPgammaS binding in rat brain sections was indistinguishable from that of HU210. Increases of similar magnitude were observed due to both agonists in the striatum, cortex, hippocampus and cerebellum. 7. ODA (10 microm) significantly inhibited forskolin-stimulated cyclic AMP (cAMP) accumulation in mouse neuroblastoma N1E 115 cells (P=0.02, n=11). ODA-mediated inhibition was completely reversed by 1 microm SR141716A (P<0.001, n=11) and was also reversed by pretreatment with 300 ng ml(-1) pertussis toxin (P<0.001, n=6). 8. These data demonstrate that ODA is a full cannabinoid CB(1) receptor agonist. Therefore, in addition to allosteric modulation of other receptors and possible entourage effects due to fatty acid amide hydrolase inhibition, the effects of ODA may be mediated directly via the CB(1) receptor.lld:pubmed
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pubmed-article:14707029pubmed:authorpubmed-author:BeckettS R...lld:pubmed
pubmed-article:14707029pubmed:authorpubmed-author:LeggettJames...lld:pubmed
pubmed-article:14707029pubmed:authorpubmed-author:D'AntonaA MAMlld:pubmed
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pubmed-article:14707029pubmed:dateRevised2011-6-7lld:pubmed
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pubmed-article:14707029pubmed:articleTitleOleamide is a selective endogenous agonist of rat and human CB1 cannabinoid receptors.lld:pubmed
pubmed-article:14707029pubmed:affiliationSchool of Biomedical Sciences, University of Nottingham Medical School, Queens Medical Centre, Nottingham, UK. mbxjdl@nottingham.ac.uklld:pubmed
pubmed-article:14707029pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:14707029pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:14707029pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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