Skip to main content
Fig. 2 | Molecular Brain

Fig. 2

From: Zonisamide can ameliorate the voltage-dependence alteration of the T-type calcium channel CaV3.1 caused by a mutation responsible for spinocerebellar ataxia

Fig. 2

Detailed analysis of the effect of ZNS on mutant CaV3.1. a Steady-state activation curves with ZNS. The normalized conductance-voltage curve was fitted to a Boltzmann equation. The activation curve of MT was shifted toward negative membrane potentials by ZNS in a concentration-dependent manner and approached the activation curve of WT. Data are presented as the mean ± S.E.M. (WT ZNS 0 [n = 9], WT ZNS 50 µM [n = 9], MT ZNS 0 [n = 11], MT ZNS 10 µM [n = 8], and MT ZNS 50 µM [n = 11]). b Comparison of the half-conductance potential. Data were obtained from the same cells shown in Fig. 1. There was a significant difference between WT and MT without ZNS (p = 0.002). In mutant CaV3.1, ZNS significantly reduced the half-conductance of the activation potential (p = 0.006). No significant difference was observed between WT without ZNS and with 50 µM ZNS (p = 0.782) and between WT without ZNS and MT with 50 µM ZNS (p = 0.625). **p < 0.01, ***p < 0.005, ns: not significant. c Comparison of the slope factor of the activation curve. There was no significant difference between WT without ZNS and each group (WT with 50 µM ZNS, p = 0.808; MT without ZNS, p = 0.110; MT with 10 µM ZNS, p = 0.677; MT with 50 µM ZNS, p = 0.614)

Back to article page