We delineated the role of Ca(2+)-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 Ca(2+). Low Ca(2+) (0.25 mM) or Cd(2+) (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 microM), a selective blocker for small-conductance Ca(2+)-activated K(+) (SK) channels. On the other hand, charybdotoxin (0.1 microM), a selective blocker for large-conductance Ca(2+)-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.

No abstract