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First published online on August 15, 2003.
Copyright © 2003 by The Physiological Society
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jphysiol.2003.050120v1
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Received June 25, 2003
Revised August 7, 2003
Accepted after revision August 11, 2003

BK channel inactivation contributes to spike broadening during repetitive firing in the rat lateral amygdala

E. S. Louise Faber1 and Pankaj Sah1*

1 Brain Research Institute, University of Queensland

* To whom correspondence should be addressed. E-mail: pankaj.sah{at}uq.edu.au.

In many neurons, trains of action potentials show frequency dependent broadening. This broadening results from the voltage dependent inactivation of potassium currents that contribute to action potential repolarisation. In different neuronal cell types these potassium currents have been shown to be either slowly inactivating delayed rectifier type currents or rapidly inactivating A-type voltage gated potassium currents. Recent findings show that inactivation of a calcium dependent potassium 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 calcium channels and BK channels. In contrast, broadening is not blocked by high concentrations 4-AP or ?-dendrotoxin. We conclude that while inactivation of BK type calcium activated potassium channels contributes spike broadening in lateral amygdala neurons, inactivation of another as yet unidentified outward current also plays a role.


Key words: Action potential • Excitability • Potassium channel







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