RECOVERY FROM C-TYPE INACTIVATION IS MODULATED BY EXTRACELLULAR POTASSIUM

Extracellular potassium modulates recovery from C-type inactivation of Kv1.3 in human T lymphocytes, The results of whole-cell patch clamp r ecordings show that there is a linear increase in recovery rate with i ncreasing [K+](o). An increase from 5 to 150 mM K-o(+) causes a sixfol d acceleration of recovery rate at a holding potential of -90 mV. Our results suggest that 1) a low-affinity K+ binding site is involved in recovery, 2) the rate of recovery increases with hyperpolarization, 3) potassium must bind to the channel before inactivation to speed its r ecovery, and 4) recovery rate depends on external [K+] but not on the magnitude of the driving force through open channels, We present a mod el in which a bound K+ ion destabilizes the inactivated state to incre ase the rate of recovery of C-type inactivation, thereby providing a m echanism for autoregulation of K+ channel activity, The ability of Kto regulate its own conductance may play a role in modulating voltage- dependent immune function.