Skip to main content
Fig. 2 | Molecular Brain

Fig. 2

From: A mutation in the low voltage-gated calcium channel CACNA1G alters the physiological properties of the channel, causing spinocerebellar ataxia

Fig. 2

Changes in electrophysiological properties. a Representative traces of T-type VDCC currents recorded from HEK293T cells expressing wild-type (upper) or mutant (lower) CaV3.1. Holding potential was -60 mV. Voltage steps were applied after a hyperpolarizing prepulse to -100 mV (duration = 500 ms). b Peak current-voltage plots of VDCC currents of wild-type (blue, n = 9) and mutant (red, n = 12) CaV3.1. c Relative conductance-voltage plots. Each data point was calculated from data in B. The black line is a fit using the Boltzmann equation (see Methods). d Steady state inactivation-voltage plots. The voltage step to -30 mV was preceded by incremental hyperpolarizing pulses (duration = 300 ms). Data were obtained from the same cells shown in B and C. The black line is a fit using the Boltzmann equation (see Methods). e The decay time constants of inactivation of the Ca2+ current plotted against voltage steps. f The 10–90 % rise times of Ca2+ currents plotted against voltage steps. Data are presented as the mean ± SEM. Statistical significance was assessed by Mann-Whitney U-test. **p < 0.01, *p < 0.05

Back to article page
\