Journal of Bioenergetics and Biomembranes

, Volume 35, Issue 6, pp 577–598

Modulation and Pharmacology of Low Voltage-Activated (“T-Type”) Calcium Channels

Authors

  • Anne Marie R. Yunker
    • Department of General Medical Sciences, E620 School of MedicineCase Western Reserve University School of Medicine
Article

DOI: 10.1023/B:JOBB.0000008025.65675.37

Cite this article as:
Yunker, A.M.R. J Bioenerg Biomembr (2003) 35: 577. doi:10.1023/B:JOBB.0000008025.65675.37

Abstract

Although T-type calcium channel currents were observed almost 30 years ago, the genes that encode the pore-forming subunits have only been recently reported. When expressed in heterologous systems, three distinct alpha1 subunits (alpha1G (Cav3.1), alpha1H (Cav3.2), and alpha1I (Cav3.3)) conduct T-type currents with insert similar but not identical electrophysiological characteristics that. Alpha1G, alpha1H, and alpha1I transcripts are found throughout neural and nonneural tissues, suggesting multiple types of T-type channels (also called low voltage-activated calcium channels (LVAs)) are coexpressed by many tissues. The study of endogenous LVAs has been hampered by a lack of highly selective antagonists that differentiate between LVA subtypes. Furthermore, many pharmacological agents attenuate currents conducted by LVA and high voltage-activated calcium channels (HVAs). At least 15 classes of pharmacological agents affect T-type currents, and the therapeutic use of many of these drugs has implicated LVAs in the etiology of a variety of diseases. Comparison of the responses of recombinant and native LVAs to pharmacological agents and endogenous modulatory molecules will lead to a better understanding of LVAs in normal and diseased cells.

T-typereviewalpha1G (Cav3.1)alpha1H (Cav3.2)alpha1I (Cav3.3)epilepsycardiacvascularpharmacology

Copyright information

© Plenum Publishing Corporation 2003