Evidence for Ca2+-activated K+ conductance in cat spinal motoneurons from intracellular EGTA injections

Ethylene glycol bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid, injected by iontophoresis from triple-barrelled intracellular micropipettes, consistently raised the membrane resistance and depressed the post-spike after hyperpolarization (AHP), but did not slow the falling phase of the action potential. [Ca2+]i-activated K+ channels appear to play a significant role in the genesis of the AHP and in the control of the resting potential, but not in the repolarization phase of the action potential.