Both intra- and extracellular injections of tetraethylammonium (TEA) prolonged the spike repolarization of motoneurons in the spinal cord of cats under pentabarbitone anaesthesia, but did not depress the afterhyperpolarization (AHP). Intracellular injections of EGTA and the fast-acting Ca2+ chelator, BAPTA, greatly depressed the AHP, but the spike shape remained unchanged. Extracellular applications of Cd2+ had similar effects. These observations suggest that a Ca2+-dependent K+ outward current is not a major mechanism of spike repolarization in motoneurons.
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