Answers are grounded in this paper and cite their sources.
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.
No takes yet. Share an insight, caveat, or question.
Krnjević et al. (1975) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: