Table 4.
cAMP Inhibition in the Presence of GAT100, Org27569, and PSNCBAM-1a
HEK-CREb | ||||||
---|---|---|---|---|---|---|
2-AG
|
AEA
|
CP55,940
|
||||
IC50 (nM) | Emax | IC50 (nM) | Emax | IC50 (nM) | Emax | |
agonist alone | 338 (203–516) | 93.6 ± 5.47 | 508 (358–719) | 87.2 ± 7.36 | 587 (474–678) | 106.3 ± 11.4 |
GAT100 | 644 (575–761)ˆ | 19.2 ± 0.95ˆˆˆ | 774 (735–805)†ˆ | 10.4 ± 1.05ˆˆˆ | 834 (786-952)† ˆ | 19.2 ± 1.62ˆˆˆ |
Org27569 | 970 (836–1180)*ˆ | 39.0 ± 1.40***ˆˆˆ | 882 (825–961)* ˆ | 28.4 ± 2.07***ˆˆˆ | 969 (829–998)* ˆ | 25.7 ± 1.64*ˆˆˆ |
PSNCBAM-1 | 978 (916–1223)*ˆ | 40.0 ± 2.13*** ˆˆˆ | 870 (849–919)* ˆ | 40.7 ± 2.45***ˆˆˆ | 962 (842–997)*ˆ | 45.7 ± 3.93***ˆˆˆ |
IC50 (nM) determined using nonlinear regression analysis; Emax (% cAMP inhibition) determined using nonlinear regression analysis. Data are mean with 95% CI (IC50) and mean ± SEM (Emax).
P < 0.05,
P < 0.01,
P < 0.001compared to GAT100 within orthosteric agonist treatment;
P < 0.05, compared to 2-AG within NAM treatment,
P < 0.05,
P < 0.01,