Abstract
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 (, J. Physiol. (Lond.). 499:3-15). Here it is shown that 1) Ba(2+) impedes the collapse of the K(+) conductance, protecting it from both sides of the membrane; 2) external Ba(2+) protection (K(d) = 63 microM at -80 mV) decreases slightly as the holding potential (HP) is made more negative; 3) external Ba(2+) cannot restore the previously collapsed conductance; on the other hand, 4) internal Ba(2+) (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). Ba(2+) is an effective K(+) substitute, inhibiting the passage of the channels into the stable nonconducting (noninactivated) mode of gating.
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Selected References
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