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1 le with that observed previously with potent cannabinoid receptor agonists.
2 esent study demonstrates that the endogenous cannabinoid receptor agonists 2-arachidonoylglycerol (2-
3 attenuated the inhibition produced by a full cannabinoid receptor agonist, (+)-[2, 3-dihydro-5-methyl
4 of several compounds as potent and selective cannabinoid receptor agonists (20, hCB(2)K(i) = 2.5 nM,
8 y examined whether systemically administered cannabinoid receptor agonists and a cannabinoid receptor
9 assessments of the physiological actions of cannabinoid receptor agonists and antagonists on adult h
12 that WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as nove
18 n the absence of exogenous agonists, and the cannabinoid receptor agonist desacetyllevonantradol fail
23 t not the undesirable side effects of direct cannabinoid receptor agonists, indicating that FAAH may
24 ndesirable side effects observed with direct cannabinoid receptor agonists, indicating that FAAH may
27 pies, such as the combined use of opioid and cannabinoid receptor agonists or selective activation of
28 acute administration of the potent synthetic cannabinoid receptor agonist R-(+)-WIN 55,212-2 (WIN; 5
30 rocannabinol (Delta(9)-THC) or the synthetic cannabinoid receptor agonist (R)-(+)-2,3-dihydro-5-methy
31 desensitized after prolonged exposure to the cannabinoid receptor agonist (R)-(+)-[2,3-dihydro-5-meth
35 ion of central nervous system (CNS)-excluded cannabinoid receptor agonists to test the hypothesis tha
37 hibition produced by Win55212-2, a synthetic cannabinoid receptor agonist, was stereoselective and wa
38 ell EPSCs were unimpaired in the presence of cannabinoid receptor agonist when the postsynaptic membr
39 ffect were observed after treatment with the cannabinoid receptor agonist WIN 55,212-2 (0.2 mg kg(-1)
40 ffect were observed after treatment with the cannabinoid receptor agonist WIN 55,212-2 (0.2 mg kg-1 i
41 We used N1E-115 neuroblastoma cells and the cannabinoid receptor agonist WIN 55,212-2 (WIN) to exami
43 effects of close-arterial injections of the cannabinoid receptor agonist WIN 55,212-2 (WIN2) on uter
44 mate release is mimicked and occluded by the cannabinoid receptor agonist WIN 55,212-2, and is abolis
48 elf-administration (SA), using the synthetic cannabinoid receptor agonist WIN55,212-2 (WIN), in order
49 arboxamide] and mimicked and occluded by the cannabinoid receptor agonist WIN55,212-2 [(beta)-(+)-[2,
50 bolished by the exogenous application of the cannabinoid receptor agonist WIN55,212-2 [R-(+)-(2,3-dih
52 n of the prototypical opioid morphine or the cannabinoid receptor agonist WIN55,212-2 produced dose-d
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