Involvement of apamin-sensitive SK channels in spike frequency adaptation of neurons in nucleus tractus solitarii of the rat

We delineated the role of Ca2+-activated K+ channels in the phenomenon of spike frequency adaptation (SFA) exhibited by neurons in the caudal region of nucleus tractus solitarius (cNTS) using intracellular recording coupled with the current-clamp technique in rat brain slices, Intracellular injection of a constant depolarizing current evoked a train of action potentials whose discharge frequency declined rapidly to a lower steady-state level of irregular discharges. This manifested phenomenon of SFA was found to be related to extracellular Ca2+. Low Ca2+ (0.25 mM) or Cd2+ (0.5 mM) in the perfusing medium resulted in a significant increase in the adaptation time constant (tau(adap)) and an appreciable reduction in the percentage adaptation of spike frequency (F-adap) in addition, the evoked discharges were converted from an irregular to a regular pattern, accompanied by a profound increase in mean firing rate. intriguingly, similar alterations in tau(adap), F-adap, discharge pattern and discharge rate were elicited by apamin (1 mu M), a selective blocker for small-conductance Ca2+-activated K+ (SK) channels. On the other hand, charybdotoxin (0.1 mu M), a selective blocker for large-conductance Ca2+-activated K+ channels, was ineffective. Our results suggest that SK channels of cNTS neurons may subserve the generation of both SFA and irregular discharge patterns displayed by action potentials evoked with a prolonged depolarizing current.