Effect of synthetic cannabinoids, endocannabinoids, and analogs on forskolin-stimulated accumulation of cAMP in BV-2 cells
| Agents | Concentration | cAMP accumulation (% of forskolin response) |
|---|---|---|
| WIN55212-2 | 1μm | 53 ± 8** |
| WIN55212-3 | 1μm | 111 ± 13 |
| AEA | 100 nM | 100 ± 7 |
| 2-AG | 100 nM | 58 ± 8** |
| PEA (16:0) | 300 nM | 60 ± 5** |
| Palmitic acid | 300 nM | 103 ± 13 |
| Acyl-EA (14:0) | 300 nM | 97 ± 11 |
| Acyl-EA (15:0) | 300 nM | 93 ± 8 |
| Acyl-EA (16:1) | 300 nM | 104 ± 10 |
| Acyl-EA (17:0) | 300 nM | 81 ± 10 |
| Acyl-EA (18:0) | 300 nM | 96 ± 17 |
| Iso-PEA | 300 nM | 122 ± 17 |
| 1-Meth-PEA | 300 nM | 116 ± 20 |
| 2-Meth-PEA | 300 nM | 118 ± 21 |
| abn-CBD | 1μm | 128 ± 11 |
| Capsaicin | 1μm | 91 ± 5 |
cAMP accumulation was measured as described in Figure 2. Agents were as follows: WIN55212-2, WIN55212-3, anandamide, 2-AG, PEA (16:0), palmitic acid, myristylethanolamide [acyl-EA (14:0)], pentadecanoylethanolamide [acyl-EA (15:0)], palmitoleylethanolamide [acyl-EA (16:1)], margaroylethanolamide [acyl-EA (17:0)], stearoylethanolamide [acyl-EA (18:0)], palmitoylisopropylamide (iso-PEA), R-palmitoyl-(1-methyl)ethanolamide (1-meth-PEA), R-palmitoyl-(2-methyl)ethanolamide (2-meth-PEA), abn-CBD, and capsaicin. Results are expressed as percentage of the forskolin response measured within individual experiments. Values are means ± SEMs of 9-36 independent quantifications of cAMP (i.e., 3-12 separate experiments performed in triplicate).
↵** p < 0.01, significantly different from forskolin response (ANOVA followed by Dunnett's post-test).