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L-type calcium channel activity regulates sodium channel levels in rat pituitary GH3 cells

E. Monjaraz, A. Navarrete, L. F. López-Santiago, A. V. Vega, J. A. Arias-Montaño and G. Cota

1. The effects of chronic pharmacological modulation of L-type Ca²⁺ channel activity on the cell surface expression of Na⁺ channels were examined in GH3 cells.

2. Prolonged inhibition (4-5 days) of L-channels with nimodipine caused a 50-60 % decrease in the peak amplitude of whole-cell Na⁺ currents recorded with the patch-clamp technique. On the contrary, prolonged exposure to the L-channel agonist Bay K 8644 induced an ~2·5-fold increase in peak Na⁺ current. In both cases, there were only minor changes in cell capacitance and no significant changes in Na⁺ channel gating properties.

3. Measurements of the specific binding of radiolabelled saxitoxin to intact cells showed that nimodipine treatment reduced the number of cell surface Na⁺ channels, whereas treatment with Bay K 8664 produced the opposite effect. The dual regulation of Na⁺ channel abundance explained the mentioned changes in Na⁺ current amplitude.

4. Plasma membrane Na⁺ channels had a half-life of ~17 h both in control cells and in cells treated with Bay K 8644, as estimated from the rate of decay of peak Na⁺ current after inhibition of protein synthesis with cycloheximide. Actinomycin D, an inhibitor of gene transcription, and also cycloheximide, occluded the stimulatory effect of Bay K 8644 on Na⁺ current density when measured over a 24 h period.

5. These findings indicate that the entry of Ca²⁺ through L-type channels influences in a positive way the number of functional Na⁺ channels in GH3 cells, and suggest that Ca²⁺ influx stimulates either Na⁺ channel gene expression or the expression of a regulatory protein that promotes translocation of pre-assembled Na⁺ channels into the plasma membrane.

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