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(Circulation Research. 2000;86:613.)
© 2000 American Heart Association, Inc.

Editorials

A Tale of Two (Calcium) Channels

Joël Nargeot

From the Institut de Genetique Humaine, Montpellier, France.

Correspondence to Joël Nargeot, Institut de Genetique Humaine, CNRS UPR 1142, 141 rue de la Cardonille, 34396-Montpellier cedex 5, France. E-mail joel.nargeot@igh.cnrs.fr

Key Words: Ca²⁺ channels • T-type channel • cardiac muscle

	Introduction

 
Calcium influx through voltage-dependent calcium channels triggers excitation-contraction coupling and regulates pacemaking activity in the heart. Two distinct families of calcium channels have been identified in cardiac tissue: L-type calcium channels, which are essential in triggering Ca²⁺ release from internal stores, and low-voltage-activated (LVA) T-type calcium channels (ICa_T), whose role remains obscure in physiological and pathophysiological conditions. Functional features of ICa_T include low threshold of activation, small unitary conductance, slow activation, and fast inactivation inducing a typical criss-crossing pattern of current traces for increasing depolarizations, negative steady-state inactivation, and slow deactivation kinetics. In addition, T-type currents compared with L-type currents are more sensitive to block by mibefradil and Ni²⁺ ions. Whereas L-type calcium channels have been extensively characterized at the functional and molecular levels, classical cloning strategies failed to identify an 1 subunit encoding for a T-type channel.

An alternative approach to identifying new members of the calcium channel family used in silico cloning strategies with a search of genetic databases for sequences homologous but not identical to known Ca²⁺ channel 1 subunits.¹ The identification of several expressed sequence tags and genomic sequences corresponding to a subset of distantly related 1 subunits resulted in the identification of full-length cDNAs encoding three distinct 1 subunits: 1G in rat,¹ mouse,² and human,^{3 4} 1H in human,^{5 6} and 1I in rat.⁷ Because 1H was obtained by screening a human heart library,⁵ it was originally considered the cardiac T-type channel isoform because of the presence in Northern blot analysis of a strong signal for . . . [Full Text of this Article]

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