Lithium transport by mouse neuroblastoma cells

Lithium entry and its distribution into veratridine-activated cells of an electrically excitable clone (N1E-115) of mouse neuroblastoma differed from that observed in resting cells. At a constant external lithium concentration, increasing the concentration of veratridine (an alkaloid which selectively activates sodium channels responsible for the generation of action potentials), resulted in a corresponding increase of both the rate of entry as well as the intracellular steady state concentration of lithium. Lithium entry occurred by a temperature dependent (Q₁₀ ∼- 1.5), formally saturable process having an apparent K_T of about 20 mM and an apparent V_max which increased from 3 nmol · (mg protein) ^-1 · (min)^-1 in the absence of veratridine to 14 nmol · (mg protein)^-1 · (min)^-1 in the presence of 0.67 mM veratridine. In both the veratridine-activated and resting states, mouse neuroblastoma cells concentrated lithium from the external medium, achieving steady state levels within 60 min; thus, in the absence of veratridine. neuroblastoma cells exhibited an intra: extracellular lithium distribution ratio of about 1.5 compared to a distribution ratio of 3.3 in the presence of 0.1 mM veratridine. Lithium accumulation in the presence of supranormal concentrations of extracellular potassium was not different from that found in controls. In addition to characterizing the differences between lithium transport found in veratridine-activated and resting cells, these results suggest that electrically active tissue may accumulate lithium to an extent proportional to the activity of the tissue.