Krnjevic_1975_Can.J.Physiol.Pharmacol_53_1214

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.