Fig. 1.

Vertebrate rhodopsin modulates GIRK and P/Q-type Ca²⁺ channels via Gi/o-PTX-sensitive pathways. (A) K⁺ current traces of GIRK1/2 channels coexpressed with RO4 or mAChR-M2 in HEK293 cells before, during, and after light stimulation (Left) or 10 μM Carb application (Right). Currents were elicited by 500-ms voltage ramps from -100 to +50 mV. (B) Comparison of the GPCR-induced current increase in the presence and absence of 5 nmol PTX. (C) Time course traces of GPCR-mediated activation of GIRK currents. GIRK currents were recorded at -60 mV. (D) Comparison of the time constants of the GPCR-induced GIRK current changes before and after GPCR activation. (E) Ba²⁺ current traces of P/Q-type Ca²⁺ channels (α₁2.1, β_1b, and α₂δ subunits) coexpressed with RO4 or mAChR-M2 in HEK293 cells before, during, and after light stimulation (Left) or 10 μM Carb application (Right). (F) GPCR-induced depolarizing shift in the voltage dependence of activation curve of P/Q-type Ca²⁺ currents. Currents were elicited from a holding potential of -60 mV by 5-ms-long, 5-mV voltage steps from -10 to +65 mV. Relative tail currents were plotted against the voltage pulses. (G) Time course traces of GPCR-mediated inhibition of P/Q-type Ca²⁺ currents. Ba²⁺ currents were elicited by voltage pulses from -60 to +20 mV and measured every s. (H) Comparison of the time constants of the GPCR-induced P/Q-type channel current changes before and after GPCR activation. Throughout all experiments number in parentheses indicate the number of experiments and statistical significance as indicated (^*, P < 0.05; ^**, P < 0.01, ANOVA).