TY - JOUR
T1 - The endocannabinoid system in rat gliosomes and its role in the modulation of glutamate release
AU - Bari, Monica
AU - Bonifacino, Tiziana
AU - Milanese, Marco
AU - Spagnuolo, Paola
AU - Zappettini, Simona
AU - Battista, Natalia
AU - Giribaldi, Francesco
AU - Usai, Cesare
AU - Bonanno, Giambattista
AU - MacCarrone, Mauro
PY - 2011/3
Y1 - 2011/3
N2 - 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-dibenzo[b,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.
AB - 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-dibenzo[b,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.
KW - Cannabinoid receptors
KW - Endocannabinoids
KW - Gliosomes
KW - Glutamate release
KW - Neuron-glia communication
KW - Vanilloid receptors
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U2 - 10.1007/s00018-010-0494-4
DO - 10.1007/s00018-010-0494-4
M3 - Article
C2 - 20711816
AN - SCOPUS:79951560770
VL - 68
SP - 833
EP - 845
JO - Cellular and Molecular Life Sciences
JF - Cellular and Molecular Life Sciences
SN - 1420-682X
IS - 5
ER -