Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells
Abstract Background Vigabatrin (VGB, y-vinyl-GABA) is an approved non-traditional antiepileptic drug that has been revealed to have the therapeutic propensity for brain tumors; however, its ionic effects in glioma cells remain unclear to a large extent. Methods With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13-06-MG. Results In cell-attached configuration, addition of VGB concentration-dependently lessened the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while subsequent application of DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) thwarted the VGB-induced inhibition of IKCa channels. Neither the activity of large-conductance Ca2+-activated (BKCa) nor that of inwardly rectifying K+ (KIR) channels was adjusted by the presence of VGB in human 13-06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusion The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an unidentified but important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.