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 (Gomez-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 (K(d) = 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.
Gómez-Lagunas, F. (1999). Barium inhibition of the collapse of the Shaker K+ conductance in zero K+. Biophysical Journal, 77(6), 2988–2998. https://doi.org/10.1016/S0006-3495(99)77130-4