NaF potentiates a K(+)-selective ion channel in G292 osteoblastic cells.
Clinical studies have established that NaF increases mineral content in bone, although the cellular mechanisms underlying its osteoinductive effects remain unclear. Because metabolic effects of fluoride have been linked to ion flux and alterations in membrane potential, we used patch-clamp recording techniques to examine the electrophysiological response of osteoblastic cells to NaF. In these experiments, we show that NaF increased the amplitude and P(open) of a 73 pS potassium-selective ion channel. The effect of NaF depended on extracellular Ca2+ and could be blocked by a combination of calcium-channel blocking agents, suggesting that potentiation of channel activity was dependent on external calcium. Because all patches were in the cell-attached configuration, the effect of NaF was presumable indirect. Although the underlying cellular mechanisms remain unclear, our findings suggest that activity of calcium and/or potassium-selective channels via second messenger cascades may mediate many of the early events involved in the response of bone cells to inorganic fluoride.
Gofa
A
A
Department of Periodontology, University of Connecticut Health Center, Farmington 06030, USA.
Davidson
R M
RM
D002121:Calcium Channel Blockers / Q000494:pharmacology; D004553:Electric Conductivity; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D009553:Nimodipine / Q000494:pharmacology; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects*; D015221:Potassium Channels / Q000187:drug effects*; D012969:Sodium Fluoride / Q000494:pharmacology*; D014407:Tumor Cells, Cultured; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D015221:Potassium Channels; D009553:Nimodipine; D012969:Sodium Fluoride; D014700:Verapamil