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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.

bmc pharmacology and toxicology

Depressive effectiveness of vigabatrin (γ-vinyl-GABA), an antiepileptic drug, in intermediate-conductance calcium-activated potassium channels in human glioma cells