Fig. 6
From: Pathophysiology of and therapeutic options for a GABRA1 variant linked to epileptic encephalopathy
Chronic, but not acute, verapamil treatment fully restored GABA-evoked chloride currents in R214C GABAAR expressing cells. a Representative traces of GABA-evoked currents from cells expressing WT or R214C GABAARs without and with verapamil (4 μM, 1 s co-applied with GABA). b Quantification of averaged peak current amplitudes recorded from cells expressing WT (n = 11) or R214C (n = 14) GABAARs without and or with verapamil. Statistical differences were determined using paired t-test (**p < 0.01, ***p < 0.001). (c) Representative traces of GABA-evoked currents from WT or R214C GABAAR expressing cells that were without (untreated) and pre-incubated with 4 μM verapamil for 24 h (Verapamil). d Quantification of averaged peak current amplitudes recorded from WT (n = 10, 12) or R214C (n = 10, 13) GABAARs that were untreated or treated with verapamil (4 μM, 24 h), respectively. Statistical differences were determined using two way ANOVA followed by post hoc student’s t-test by comparing GABA-evoked currents of untreated WT GABAAR expressing cells (***p < 0.001), or untreated R214C GABAAR expressing cells (###p < 0.001). e Dose-response curve for GABA-evoked currents from R214C GABAAR expressing cells pre-treated with 4 μM verapamil for 24 h (n = 12). The dose curve for verapamil treated (4 μM, 24 h) R214C GABAARs was replotted against the dose response curve in Fig. 3. The peak current amplitudes at each GABA concentrations were normalized to the maximum responses from WT GABAAR (1 mM GABA). Statistical differences were determined using student’s t-test by comparing to the GABA-evoked currents from WT (*p < 0.05, **p < 0.01, ***p < 0.001), or R214C (###p < 0.001), at the corresponding GABA concentration. Data is represented as +SEM