Batrachotoxin modifies the gating kinetics of sodium channels in internally perfused neuroblastoma cells.

AUTOR(ES)

Huang, L Y

RESUMO

We have studied the effects of batrachotoxin (BTX) on sodium channels in hybrid mouse neuroblastoma cells NG108-15 by using the suction pipet voltage clamp method. BTX-modified sodium channels activate with first-order kinetics and, over most of the potential range, activate more slowly than normal sodium channels. The peak conductance-voltage curve and the time constant of activation-versus-voltage curve for BTX-modified sodium channels are shifted about 50 mV in the hyperpolarizing direction compared to the corresponding curves for normal sodium channels. There is no change in the slope of the conductance-voltage curve. These results suggest that BTX slows down one of the steps leading to channel opening, which consequently becomes rate-limiting. In addition, BTX eliminates both fast and slow inactivation.

Documentos Relacionados

• Burst kinetics of sodium channels which lack fast inactivation in mouse neuroblastoma cells.
• Specific monosaccharide inhibition of active sodium channels in neuroblastoma cells.
• Open-channel block by internally applied amines inhibits activation gate closure in batrachotoxin-activated sodium channels.
• Modification of cardiac Na+ channels by batrachotoxin: effects on gating, kinetics, and local anesthetic binding.
• Differential block of sodium and calcium channels by chlorpromazine in mouse neuroblastoma cells.