Gating charges per channel of Ca(V)2.2 channels are modified by G protein activation in rat sympathetic neurons
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Updated: Jun 24, 2026

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
Published on: July 17, 2011
Santiago Rebolledo-Antúnez1, José M Farías, Isabel Arenas
1Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Av. Universidad 3000, Ciudad Universitaria, Delegación Coyoacán, C.P. 04510, Apdo. Postal 70250, México, D.F., Mexico.
Abstract:
It has been suggested that voltage-dependent G protein modulation of Ca(V)2.2 channels is carried out at closed states of the channel. Our purpose was to estimate the number of gating charges of Ca(V)2.2 channel in control and G protein-modulated conditions. By using a Cole-Moore protocol we observed a significant delay in Ca(V)2.2 channel activation according to a transit of the channel through a series of closed states before channel opening. If G protein voltage-dependent modulation were carried out at these closed states, then we would have expected a greater Cole-Moore lag in the presence of a neurotransmitter. This prediction was confirmed for noradrenaline, while no change was observed in the presence of angiotensin II, a voltage-insensitive G protein modulator. We used the limiting slope method for calculation of the gating charge per channel. Effective charge z was 6.32+/-0.65 for Ca(V)2.2 channels in unregulated conditions, while GTPgammaS reduced elementary charge by approximately 4 e(0). Accordingly, increased concentration of noradrenaline induced a gradual decrease on z, indicating that this decrement was due to a G protein voltage-sensitive modulation. This paper shows for the first time a significant and reversible decrease in charge transfer of Ca(V)2.2 channels under G protein modulation, which might depend on the activated G protein inhibitory pathway.
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