Figure 5.

AB‐CHMINACA does not modulate cAMP levels via CB1 receptors in HEK 293 cells. A, Treatment with AB‐CHMINACA produced a concentration‐dependent increase in forskolin‐mediated cAMP production in HEK 293‐CB1 in presence of PTX. B, Traces from a representative experiment showing that AB‐CHMINACA (10 µmol L⁻¹) induced observed stimulatory effects were only partially inhibited by SR141716A 3 µmol L⁻¹. C, Scatter dot plot comparing AB‐CHMINACA‐mediated stimulation of forskolin (3 μmol L⁻¹)‐induced cAMP response in presence and absence of SR141716 3 µmol L⁻¹ in HEK 293‐CB1 cells, and the data were not significantly different. AB‐CHMINACA (10 µmol L⁻¹) also modestly augmented forskolin‐stimulated cAMP levels in HEK‐wild‐type cells (not containing CB1 receptors). Graphs show mean ± SEM for at least five independent experiments performed in duplicate. cAMP, cyclic adenosine monophosphate; CB1, cannabinoid receptor type 1; HEK, human embryonic kidney; PTX, pertussis toxin