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Biophys J, December 1999, p. 2988-2998, Vol. 77, No. 6
Departamento de Reconocimiento Molecular y Biologia Estructural, Instituto de Biotecnologia, UNAM, Cuernavaca, Morelos 62250, and Departamento de Fisiologia, Facultad de Medicina, UNAM, D.F. 04510, Mexico
In the absence of K+ on both sides of the
membrane, delivery of standard activating pulses collapses the
Shaker B K+ conductance. Prolonged
depolarizations restore the ability to conduct K+. It has
been proposed that the collapse of the conductance results from the
dwelling of the channels in a stable closed (noninactivated) state
(Gómez-Lagunas, 1997, J. Physiol. (Lond.).
499:3-15). Here it is shown that 1) Ba2+ impedes the
collapse of the K+ conductance, protecting it from both
sides of the membrane; 2) external Ba2+ protection
(Kd = 63 µM at
80 mV) decreases
slightly as the holding potential (HP) is made more negative; 3)
external Ba2+ cannot restore the previously collapsed
conductance; on the other hand, 4) internal Ba2+ (and
K+) protection markedly decreases with hyperpolarized HPs
(
80 to
120 mV), and it is not dependent on the pulse potential (0 to +60 mV). Ba2+ is an effective K+ substitute,
inhibiting the passage of the channels into the stable nonconducting
(noninactivated) mode of gating.
Biophys J, December 1999, p. 2988-2998, Vol. 77, No. 6
© 1999 by the Biophysical Society 0006-3495/99/12/2988/11 $2.00
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