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Journal of Neuroscience, Vol 16, 586-594, Copyright © 1996 by Society for Neuroscience
A slowly inactivating potassium current in CA3 pyramidal cells of rat hippocampus in vitro
A Luthi, BH Gahwiler and U Gerber
Brain Research Institute, University of Zurich, Switzerland.
The time- and voltage-dependent properties of a slowly inactivating K+
current were investigated by using the single-electrode current- and
voltage-clamp recording technique in CA3 hippocampal cells of organotypic
slice cultures. After a period of prolonged hyperpolarization, the onset of
action-potential discharge in response to depolarizing current injection
was delayed by several seconds. The conductances underlying this delay were
identified in voltage-clamp recordings. A biphasically decaying outward
current was evoked when the membrane potential was stepped back to -60 mV
after a 30 sec period of hyperpolarization. The fast component was
identified as the previously described D-current and was blocked by 100
microM 4-aminopyridine (4- AP). The slow component, which we refer to as
IK(slow), appeared to be mediated by K+ ions, because its reversal
potential shifted in a Nernstian manner with changes in extracellular K+
concentration. It decayed with a time constant of 7.5 sec and required a
hyperpolarizing prepulse below -95 mV for 5.5 sec for 50% recovery from
inactivation. IK(slow) was found to be voltage-dependent, with 50%
activation occurring at -65 mV and 50% steady-state inactivation occurring
at -84 mV. It displayed minimal or no sensitivity to the K(+)-channel
blockers 4-AP (0.1-5 mM), Cs+ (1 mM), tetraethylammonium (10-50 mM), Ba2+
(1 mM), dendrotoxin-alpha (5-10 microM), charybdotoxin (0.5-2.5 microM), or
glibenclamide (5-10 microM) and was not affected by preventing increases in
intracellular Ca2+ concentration with Ca2+ chelators. IK(slow) was reduced
by activation of metabotropic glutamatergic and cholinergic receptors. In
summary, the biophysical characteristics of IK(slow) suggest a role in
determining discharge onset after a period of membrane hyperpolarization,
and its modulation by G-protein-coupled receptors reveals an additional
function for these receptors in the control of cellular excitability.
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