Figure 2.
Agonist-induced structural rearrangements in the GB1aR/G-protein/CaV2.2 channel complex. A, E between GB1aYFP/CaV2.2CFP was reduced by baclofen (10 μm, left, n = 13–29, N = 4–6, ***p < 0.0001), but was increased by CGP54626 (1 μm, right, n = 14, N = 4, **p < 0.01). B, E between GB1aYFP/GαoCFP was reduced by baclofen (10 μm, left, n = 12–17, N = 4, ***p < 0.0001), but was increased by GABABR antagonist CGP35348 (1 μm, right, n = 13–18, N = 4, ***p < 0.0001). C, E between GB1aCFP/Gβ1YFP was increased by baclofen (10 μm, left, n = 12–15, N = 4, ***p < 0.0001), but was decreased by GABABR antagonist CGP54626 (1 μm, right, n = 15, N = 4, ***p < 0.0001). D, E between Gβ1YFP/CaV2.2CFP was increased by baclofen (10 μm, left, n = 14–27, N = 4–6, ***p < 0.0001), but was decreased by CGP54626 (1 μm, right, n = 14–17, N = 4–5, ***p < 0.0001). Error bars indicate SEM. E, Fluorescence intensity of pHluorin tagged to GB1a does not change under miniature activity, by application of 10 μm baclofen and as function of stimulation frequency (10 and 100 Hz). Slope of linear fit is 1.04, 0.98, 1.01, and 0.99 for miniature activity, baclofen application, 10 and 100 Hz, respectively.