Involvement of Apamin-Sensitive SK Channels in Spike Frequency Adaptation of Neurons in Nucleus tractus solitarii of the Rat

Abstract

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.

A Neuro-hormonal Circuit for Paternal Behavior Controlled by a Hypothalamic Network Oscillation

“…Here we show that Prl excites presynaptic inputs of MPOA Gal + neurons (Figures 4J and 4K) and that it mediates its actions at least in part via a post-synaptic effect (Figures 4L and 4M). Identification of SK channel inhibition as the mechanism underlying the postsynaptic action of Prl (Figures 4L and 4M) can explain the emergence of high-frequency firing in MPOA Gal + neurons in the presence of the hormone (Figure 4H; Ellis et al, 2007;Yen et al, 1999) and, consequently, increased network output. It remains to be determined whether Prl acts on all MPOA Gal + subsets or whether it is biased toward some of the functional subgroups identified by .…”