The endocannabinoid system in rat gliosomes and its role in the modulation of glutamate release |
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Authors: | Monica Bari Tiziana Bonifacino Marco Milanese Paola Spagnuolo Simona Zappettini Natalia Battista Francesco Giribaldi Cesare Usai Giambattista Bonanno Mauro Maccarrone |
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Institution: | 1.Centro Europeo per la Ricerca sul Cervello (CERC)/Fondazione Santa Lucia,Rome,Italy;2.Dipartimento di Medicina Sperimentale e Scienze Biochimiche,Università degli Studi di Roma “Tor Vergata”,Rome,Italy;3.Dipartimento di Medicina Sperimentale, Sezione di Farmacologia e Tossicologia e Centro di Eccellenza per la Ricerca Biomedica,Università degli Studi di Genova,Genoa,Italy;4.Dipartimento di Scienze Biomediche,Università degli Studi di Teramo,Teramo,Italy;5.Istituto di Biofisica,Consiglio Nazionale delle Ricerche,Genoa,Italy;6.Istituto Nazionale di Neuroscienze,Turin,Italy;7.Department of Pharmacobiology,University of Calabria,Cosenza,Italy |
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Abstract: | The endocannabinoid system and endocannabinoid receptor-driven modulation of glutamate release were studied in rat brain cortex
astroglial gliosomes. These preparations contained the endocannabinoids N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol, as well their major biosynthetic (N-acyl-phosphatidylethanolamines-hydrolyzing-phospholipase D and diacylglycerol-lipase) and catabolic (fatty acid amide-hydrolase
and monoacylglycerol-lipase) enzymes. Gliosomes expressed type-1 (CB1R), type-2 (CB2R) cannabinoid, and type-1 vanilloid (TRPV1)
receptors, as ascertained by Western blotting and confocal microscopy. Methanandamide, a stable analogue of anandamide acting
as CB1R, CB2R, and TRPV1 agonist, stimulated or inhibited the depolarization-evoked gliosomal 3H]d-aspartate release, at lower and higher concentrations, respectively. Experiments with ACEA (arachidonyl-2′-chloroethylamide),
JWH133 ((6aR,10aR)-3-(1,1-dimethylbutyl)-6a,7,10,10a-tetrahydro-6,6,9-trimethyl-6H-dibenzob,d]-pyran) and capsaicin, selective
agonists at CB1R, CB2R and TRPV1, respectively, demonstrated that potentiation of 3H]d-aspartate release was due to CB1R while inhibition to CB2R and TRPV1 engagement. These findings were confirmed by using selective
receptor antagonists. Furthermore, CB1R activation caused increase of intracellular IP3 and Ca2+ concentration, suggesting an involvement of phospholipase C. |
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