G-protein-coupled receptors (GPCR) control neuronal functions via ion channel modulation. For voltage-gated ion channels, gating charge movement precedes and underlies channel opening. Therefore we sought to investigate the effects of G-protein activation on gating charge movement. Non-linear capacitive currents were recorded using the whole-cell patch-clamp technique in cultured rat sympathetic neurons. Our results show that gating charge movement depends on voltage with average Boltzmann parameters: Q_max = 6.1 ± 0.6 nC/µF, V_h = --29.2 ± 0.5 mV and k = 8.4 ± 0.4 mV. Intracellular dialysis with GTPS produces a non-reversible, ~34% decrease in Q_max, a ~10 mV shift in V_h, and a ~63% increase in k with respect to the control. Noradrenaline (NA) induces a ~7 mV shift in V_h and ~40% increase in k. Overexpression of G-protein 14 subunits produces a ~13% decrease in Qmax, a ~9 mV shift in V_h, and a ~28% increase in k. We correlate charge movement modulation with the modulated behavior of voltage-gated channels. Concurrently, G-protein activation by transmitters and GTPS also inhibit both Na⁺ and N-type Ca²⁺ channels. These results reveal an inhibition of gating charge movement by G-protein activation that parallels the inhibition of both Na⁺ and N-type Ca²⁺ currents. We propose that gating charge movement decrement may precedes or accompanies some forms of GPCR-mediated channel current inhibition or down regulation. This may be a common step in the GPCR-mediated inhibition of distinct populations of voltage-gated ion channels.