EGTA and motoneuronal after‐potentials.

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Abstract
Intracellular iontophoretic injections of EGTA [ethylene glycol bis(.beta.-aminoethylether)-N,N''-tetraacetic acid] (5-20 nA) into cat spinal motoneurones consistently greatly reduced the amplitude of the delayed after-hyperpolarization (AHP) that followed the spike. This effect was accompanied by a large reduction (on average by 3/4) in the marked increase in input conductance normally associated with the AHP. There was also a consistent, though less regular, tendency for the resting input conductance to decrease (on average by 1/5), and some depolarization. Recovery of the AHP, the associated conductance increase and the resting conductance was very slow. It was sometimes accelerated by injections of citrate and Cl-, or Ca2+. Other hyperpolarizing phenomena, such as recurrent or othodromically-evoked IPSP [inhibitory postsynaptic potential], are not depressed by injections of EGTA. When depolarization is minimal, EGTA injections that markedly depress the AHP did not affect the rate of rise or fall of the spike. If, as a result of depolarization, an early AHP was visible, it was patently insensitive to EGTA. The post-spike depolarizing after-potential (delayed depolarization) was not obviously affected by EGTA, apart from the usual diminution seen during depolarization. Since the main action of EGTA is to bind free Ca2+, the marked depression of the AHP indicates that the sharp increase in K+ conductance which generates the AHP is probably caused by an influx of Ca2+ accompanying the action potential. This inward Ca2+ current may be manifested in the depolarizing after-potential.