Delayed rectifying and calcium-activated K⁺ channels and their significance for action Potential Repolarization in Mouse pancreatic β-cells

The contribution of Ca²⁺-activated and delayed rectifying K⁺ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic β-cells (Rorsman, P., and G. Trube. 1986. J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca²⁺-dependent component could be identified by its rapid inactivation and sensitivity to the Ca²⁺ channel blocker Cd²⁺. This current showed the same voltage dependence as the voltage-activated (Cd²⁺-sensitive) Ca²⁺ current and contributed 10-20% to the total β-cell delayed outward current. The single-channel events underlying the Ca²⁺-activated component were investigated in cell-attached patches. Increase of [Ca²⁺]_i invariably induced a dramatic increase in the open state probability of a Ca²⁺-activated K⁺ channel. This channel had a single-channel conductance of 70 pS ([K⁺]_o = 5.6 mM). The Ca²⁺-independent outward current (constituting >80% of the total) reflected the activation of an 8 pS ([K⁺]_o = 5.6 mM; [K⁺]_i = 155 mM) K⁺ channel. This channel was the only type observed to be associated with action potentials in cell-attached patches. It is suggested that in mouse β-cells spike repolarization results mainly from the opening of the 8-pS delayed rectifying K⁺ channel.