Abstract
BACKGROUND: Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. 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, VGB concentration-dependently reduced the activity of intermediate-conductance Ca(2+)-activated K(+) (IK(Ca)) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IK(Ca) channels. However, the activity of neither large-conductance Ca(2+)-activated (BK(Ca)) nor inwardly rectifying K(+) (K(IR)) channels were affected by the presence of VGB in human 13-06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl(2) effectively suppressed BK(Ca) and K(IR) channels. CONCLUSIONS: The inhibitory effect of VGB on IK(Ca) channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.