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Physiological Reviews, Vol. 83, No. 1, January 2003, pp. 117-161; 10.1152/physrev.00018.2002.
Copyright ©2003 by the American Physiological Society
Department of Pharmacology, University of Virginia, Charlottesville, Virginia
Perez-Reyes, Edward
Molecular Physiology of Low-Voltage-Activated T-type
Calcium Channels. Physiol. Rev. 83: 117-161, 2003.
T-type
Ca2+ channels were originally called low-voltage-activated
(LVA) channels because they can be activated by small depolarizations of the plasma membrane. In many neurons Ca2+ influx through
LVA channels triggers low-threshold spikes, which in turn triggers
a burst of action potentials mediated by Na+ channels.
Burst firing is thought to play an important role in the synchronized
activity of the thalamus observed in absence epilepsy, but may also
underlie a wider range of thalamocortical dysrhythmias. In addition to
a pacemaker role, Ca2+ entry via T-type channels can
directly regulate intracellular Ca2+ concentrations, which
is an important second messenger for a variety of cellular processes.
Molecular cloning revealed the existence of three T-type channel
genes. The deduced amino acid sequence shows a similar four-repeat
structure to that found in high-voltage-activated (HVA)
Ca2+ channels, and Na+ channels, indicating
that they are evolutionarily related. Hence, the
1-subunits of T-type channels are now designated
Cav3. Although mRNAs for all three Cav3
subtypes are expressed in brain, they vary in terms of their peripheral
expression, with Cav3.2 showing the widest expression. The
electrophysiological activities of recombinant Cav3
channels are very similar to native T-type currents and can be
differentiated from HVA channels by their activation at lower voltages,
faster inactivation, slower deactivation, and smaller conductance of
Ba2+. The Cav3 subtypes can be differentiated
by their kinetics and sensitivity to block by Ni2+. The
goal of this review is to provide a comprehensive description of
T-type currents, their distribution, regulation, pharmacology, and cloning.
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