Literature DB >> 23708835

ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K⁺ o-dependent resting inactivation.

Yen May Cheng1, David Fedida, Steven J Kehl.   

Abstract

Previous studies have shown that in N-type inactivation-removed Shaker (ShakerIR) channels, the T449K and T449A mutations result in enhanced slow inactivation. These mutant channels also show a loss of conductance in 0 mM K⁺ o that was attributed to an inactivation process occurring from the closed, resting state and which we refer to as resting inactivation. Similar behavior has also been observed in the Kv1.5 H463G mutant channel. To date, the time courses for the onset of and recovery from resting inactivation have been unknown, but a comparison of the kinetics for resting inactivation induced at -80 mV and slow inactivation evoked at +50 mV may provide information on whether these two processes are mechanistically related. Here, we present an analysis of the time courses for the onset of and recovery from [K⁺]o-dependent resting inactivation and depolarization-induced inactivation of these mutant channels. Despite the enhancement of slow inactivation in the ShakerIR T449K, T449A, and Kv1.5 H463G mutants, the time constant for slow inactivation at +50 mV (τ inact) was relatively insensitive to the increases or decreases of [K(+)]o, confirming that accelerated inactivation from the open state does not underlie the loss of conductance in 0 mM K⁺. For all three mutants, the time constant for resting inactivation (τ RI), induced by exposure to 0 mM K⁺ o solution at -80 mV, was at least an order of magnitude larger than τ inact. On the other hand, the time course of recovery at -80 mV of each mutant from 0 mM K(+) o-induced resting inactivation was the same as that from depolarization-induced slow inactivation. This latter result suggests that the 0 mM K⁺ o-induced resting inactivation of these mutant ShakerIR and Kv1.5 channels is mechanistically related to slow inactivation.

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Year:  2013        PMID: 23708835     DOI: 10.1007/s00424-013-1297-x

Source DB:  PubMed          Journal:  Pflugers Arch        ISSN: 0031-6768            Impact factor:   3.657


  43 in total

1.  Extracellular K+ specifically modulates a rat brain K+ channel.

Authors:  L A Pardo; S H Heinemann; H Terlau; U Ludewig; C Lorra; O Pongs; W Stühmer
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2.  Kinetic analysis of the effects of H+ or Ni2+ on Kv1.5 current shows that both ions enhance slow inactivation and induce resting inactivation.

Authors:  Yen May Cheng; David Fedida; Steven J Kehl
Journal:  J Physiol       Date:  2010-06-25       Impact factor: 5.182

3.  Loss of shaker K channel conductance in 0 K+ solutions: role of the voltage sensor.

Authors:  A Melishchuk; A Loboda; C M Armstrong
Journal:  Biophys J       Date:  1998-10       Impact factor: 4.033

4.  [K+]out accelerates inactivation of Shal-channels responsible for A-current in rat CA1 neurons.

Authors:  Y V Kirichok; A V Nikolaev; O A Krishtal
Journal:  Neuroreport       Date:  1998-03-09       Impact factor: 1.837

5.  A voltage-dependent role for K+ in recovery from C-type inactivation.

Authors:  D I Levy; C Deutsch
Journal:  Biophys J       Date:  1996-12       Impact factor: 4.033

6.  TEA prevents inactivation while blocking open K+ channels in human T lymphocytes.

Authors:  S Grissmer; M Cahalan
Journal:  Biophys J       Date:  1989-01       Impact factor: 4.033

7.  Dilated and defunct K channels in the absence of K+.

Authors:  A Loboda; A Melishchuk; C Armstrong
Journal:  Biophys J       Date:  2001-06       Impact factor: 4.033

8.  Effects of changes in extracellular pH and potassium concentration on Kv1.3 inactivation.

Authors:  Sándor Somodi; Péter Hajdu; Rezso Gáspár; György Panyi; Zoltán Varga
Journal:  Eur Biophys J       Date:  2008-01-24       Impact factor: 1.733

9.  The inactivation behaviour of voltage-gated K-channels may be determined by association of alpha- and beta-subunits.

Authors:  S Heinemann; J Rettig; V Scott; D N Parcej; C Lorra; J Dolly; O Pongs
Journal:  J Physiol Paris       Date:  1994

10.  Functional consequences of a decreased potassium affinity in a potassium channel pore. Ion interactions and C-type inactivation.

Authors:  E M Ogielska; R W Aldrich
Journal:  J Gen Physiol       Date:  1999-02       Impact factor: 4.086

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  1 in total

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Authors:  Kevin R Novak; Jennifer Norman; Jacob R Mitchell; Martin J Pinter; Mark M Rich
Journal:  Ann Neurol       Date:  2015-01-09       Impact factor: 10.422

  1 in total

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