Sodium-activated potassium conductance participates in the depolarizing afterpotential following a single action potential in rat hippocampal CA1 pyramidal cells

Abstract

The depolarizing afterpotential (DAP) following an action potential increases the excitability of a neuron. Mechanisms related to the DAP following an antidromic or current-induced spike were studied in CA1 pyramidal cells by whole-cell recordings in hippocampal slices in vitro. In DAP-holding voltage curves, the DAP at 10 ms after the spike peak (DAP10) was extrapolated to reverse at about −50 mV. Increase of extracellular K + concentration increased DAP and neuronal bursting. DAP10 reversal potential shifted positively with an increase in [K +] o and with the blockade of K + conductance using pipettes filled with Cs +. Similarly, extracellular tetraethylammonium (TEA; 10 mM), 4-aminopyridine (3–10 mM) increased DAP and shifted the DAP10 reversal potential to a depolarizing direction. Decrease of [Ca 2+] o did not alter DAP significantly, suggesting a nonessential role of Ca 2+ in the DAP. Perfusion of tetrodotoxin (TTX; 0.1–1 μM) and replacement of extracellular Na + by choline + suppressed both spike height and DAP simultaneously. Replacement of extracellular Na + by Li + increased DAP and spike bursts, and caused a positive shift of the DAP10 reversal potential. It is suggested that Li + increased DAP by blocking an Na +-activated K + current. In summary, multiple K + conductances are normally active during the DAP following a single action potential.