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Ca 2+ ‐activated K + (BK) channel inactivation contributes to spike broadening during repetitive firing in the rat lateral amygdala
Author(s) -
Faber E. S. Louise,
Sah Pankaj
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2003.00483.x
Subject(s) - spike (software development) , amygdala , bk channel , neuroscience , biophysics , chemistry , potassium channel , psychology , biology , computer science , software engineering
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 Ca 2+ ‐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 Ca 2+ 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 Ca 2+ ‐activated K + channels contributes to spike broadening in lateral amygdala neurons, inactivation of another as yet unidentified outward current also plays a role.