Ca2+ -activated K+ (BK) channel inactivation contributes to spike broadening during repetitive firing in the rat lateral amygdala

E. S.Louise Faber, Pankaj Sah*

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    100 Citations (Scopus)

    Abstract

    In many neurons, trains of action potentials show frequency-dependent broadening. This broadening results from the voltage-dependent inactivation of K+ currents that contribute to action potential repolarisation. In different neuronal cell types these K+ currents have been shown to be either slowly inactivating delayed rectifier type currents or rapidly inactivating A-type voltage-gated K+ currents. Recent findings show that inactivation of a Ca2+-dependent K+ current, mediated by large conductance BK-type channels, also contributes to spike broadening. Here, using whole-cell recordings in acute slices, we examine spike broadening in lateral amygdala projection neurons. Spike broadening is frequency dependent and is reversed by brief hyperpolarisations. This broadening is reduced by blockade of voltage-gated Ca2+ channels and BK channels. In contrast, broadening is not blocked by high concentrations of 4-aminopyridine (4-AP) or α-dendrotoxin. We conclude that while inactivation of BK-type Ca2+-activated K+ channels contributes to spike broadening in lateral amygdala neurons, inactivation of another as yet unidentified outward current also plays a role.

    Original languageEnglish
    Pages (from-to)483-497
    Number of pages15
    JournalJournal of Physiology
    Volume552
    Issue number2
    DOIs
    Publication statusPublished - 15 Oct 2003

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