Abstract
To elucidate molecular mechanisms of neurotropic action of a recombinant interferon, IFN-α2b (laferon), its effect on transport of 22Na+ through the membrane of cultured human neuroblastoma cells (line IMR 32) was investigated. Within the first minutes after treatment with IFN-α2b, the influx of 22Na+ ions was reduced by 20%, as compared with the control. Depolarization of the plasma membrane by a mixture of veratrine and scorpion (Leiurus quinquestriatus) toxin (200 and 10 μg/ml, respectively) increased this flux by 50% in the control and by 70% in the IFN-α2b-treated cells. A blocker of voltage-operated sodium channels, tetrodotoxin (TTX, 4 · 10-7 M), suppressed the inward flux of 22Na+ ions (completely in the control cells and by 75% in the IFN-α2b-treated cells). The influx of 22Na+ ions into neuroblastoma cells depended on the concentration of IFN-α2b in the incubation medium, reaching a maximum at concentrations of 600-1000 IU/ml. This allows us to suggest that entry of Na+ ions into neuroblastoma cells caused by IFN-α2b is basically performed through voltage-operated TTX-sensitive sodium channels.
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