Comparison of the Ca2 +  currents induced by expression of three cloned α1 subunits, α1G, α1H and α1I, of low-voltage-activated T-type Ca2 +  channels

Authors

  • Udo Klöckner,

    1. Institute of Vegetative Physiology, University of Cologne, Robert-Koch-Strasse 39, D-50931 Köln, Germany
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  • Jung-Ha Lee,

    1. Department of Physiology, Loyola University Medical Center, 2160 South First Avenue, Maywood, Illinois, 60153, USA
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    • Present address: Pharmacology, University of Virginia, Box 448 Jordan Hall, Charlottesville, VA 22908, USA

  • Leanne L. Cribbs,

    1. Department of Physiology, Loyola University Medical Center, 2160 South First Avenue, Maywood, Illinois, 60153, USA
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  • Asif Daud,

    1. Department of Physiology, Loyola University Medical Center, 2160 South First Avenue, Maywood, Illinois, 60153, USA
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  • Jürgen Hescheler,

    1. Institute of Neurophysiology, University of Cologne, Robert-Koch-Strasse 39, D-50931 Köln, Germany
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  • Alexei Pereverzev,

    1. Institute of Neurophysiology, University of Cologne, Robert-Koch-Strasse 39, D-50931 Köln, Germany
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  • Edward Perez-Reyes,

    1. Department of Physiology, Loyola University Medical Center, 2160 South First Avenue, Maywood, Illinois, 60153, USA
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    • Present address: Pharmacology, University of Virginia, Box 448 Jordan Hall, Charlottesville, VA 22908, USA

  • Toni Schneider

    1. Institute of Neurophysiology, University of Cologne, Robert-Koch-Strasse 39, D-50931 Köln, Germany
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: Dr Toni Schneider, as above.
E-mail: TS@physiologie.uni-koeln.de

Abstract

Expression of rat α1G, human α1H and rat α1I subunits of voltage-activated Ca2 +  channels in HEK-293 cells yields robust Ca2 +  inward currents with 1.25 mm Ca2 +  as the charge carrier. Both similarities and marked differences are found between their biophysical properties. Currents induced by expression of α1G show the fastest activation and inactivation kinetics. The α1H and α1I currents activate and inactivate up to 1.5- and 5-fold slower, respectively. No differences in the voltage dependence of steady state inactivation are detected. Currents induced by expression of α1G and α1H deactivate with time constants of up to 6 ms at a test potential of − 80 mV, but currents induced by α1I deactivate about three-fold faster. Recovery from short-term inactivation is more than three-fold slower for currents induced by α1H and α1I in comparison to α1G. In contrast to these characteristics, reactivation after long-term inactivation was fastest for currents arising from expression of α1I and slowest in cells expressing α1H calcium channels. The calcium inward current induced by expression of α1I is increased by positive prepulses while currents induced by α1H and α1G show little ( <  5%) or no facilitation. The data thus provide a characteristic fingerprint of each channel's activity, which may allow correlation of the α1G, α1H and α1I induced currents with their in vivo counterparts.

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