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

J. C. Yen, Julie Y.H. Chan, Samuel H.H. Chan*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

13 Scopus citations

Abstract

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 steadystate level of irregular discharges. This manifested phenomenon of SFA was found to be related to extracellular Ca2+. Low Ca2+ (0.25 mM) or Cd2+2+ (0.5 mM) in the perfusing medium resulted in a significant increase in the adaptation time constant (τ(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 τ(adap), F(adap), discharge pattern and discharge rate were elicited by apamin (1 μM), a selective blocker for small-conductance Ca2+- activated K+ (SK) channels. On the other hand, charybdotoxin (0.1 μM), 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.

Original languageEnglish
Pages (from-to)418-424
Number of pages7
JournalJournal of Biomedical Science
Volume6
Issue number6
DOIs
StatePublished - 1999
Externally publishedYes

Keywords

  • Apamin
  • Charybdotoxin
  • Nucleus tractus solitarii
  • Spike frequency adaptation

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