Region | Treatment | WT mice | S426A/S430A mice | ||
---|---|---|---|---|---|
Emax (fmol/mg) | EC50 (nm) | Emax (fmol/mg) | EC50 (nm) | ||
PAG | Vehicle | 169.6 ± 13.8 | 8.6 ± 1.3 | 151.0 ± 15.9 | 17.4 ± 2.8* |
PAG | Δ9-THC | 114.6 ± 8.5† | 11.8 ± 1.9 | 146.8 ± 11.6 | 18.6 ± 2.0 |
Spinal cord | Vehicle | 75.8 ± 4.4 | 10.5 ± 1.1 | 69.0 ± 5.3 | 13.1 ± 2.3 |
Spinal cord | Δ9-THC | 67.7 ± 4.0 | 20.3 ± 3.6† | 67.3 ± 6.1 | 14.3 ± 3.1 |
Hippocampus | Vehicle | 177.0 ± 6.9 | 5.4 ± 0.9 | 155.5 ± 9.9 | 5.8 ± 0.9 |
Hippocampus | Δ9-THC | 145.2 ± 9.0† | 6.1 ± 0.8 | 147.5 ± 8.4 | 11.1 ± 3.5 |
Data are mean Emax (net-stimulated fmol/mg) and EC50 values ± SEM (n = 5–6) derived from the concentration–effect curves from Figure 3, which were fit by nonlinear regression. Membranes from the indicated CNS regions of vehicle- and THC-treated WT and S426A/S430A CB1 receptor knock-in mice were incubated with 30 μm GDP, 0.1 nm [35S]GTPγS, and varying concentrations of CP55,940, as described in Materials and Methods.
↵*p < 0.05 different from wild-type mice of the same treatment group as determined by ANOVA and planned comparison with Bonferroni post hoc test.
↵†p < 0.05 different from vehicle-treated mice of the same genotype as determined by two-way ANOVA and planned comparison with Bonferroni post hoc test.