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Ca(v)1.3 and BK channels for timing and regulating cell firing
David Henry Vandael1, Andrea Marcantoni, Satyajit Mahapatra
1Department of Neuroscience, NIS Centre, CNISM, Corso Raffaello 30, 10125 Turin, Italy.
Molecular Neurobiology
|November 20, 2010
Summary
Calcium-channel Ca(v)1.3 (LTCCs) are crucial for pacemaker activity in excitable cells. This review details Ca(v)1.3 gating and its coupling with BK channels in regulating cell firing.
Area of Science:
- Electrophysiology
- Molecular and Cellular Physiology
- Neuroscience
Background:
- L-type Ca(2+) channels (LTCCs, Ca(v)1) regulate cell excitability and Ca(2+)-dependent processes.
- Ca(v)1.3, an LTCC isoform, supports pacemaker currents due to its activation kinetics.
Purpose of the Study:
- To review Ca(v)1.3 channel gating mechanisms.
- To explore the coupling of Ca(v)1.3 with large conductance BK channels.
- To provide a unified view of their roles in regulating cell excitability.
Main Methods:
- Utilized Ca(v)1.3 knockout mice.
- Employed membrane current recording techniques, including dynamic and action potential clamp.
- Investigated Ca(v)1.3 pacemaker currents in dopaminergic neurons and adrenal chromaffin cells.
Main Results:
- Resolved the time course of Ca(v)1.3 pacemaker currents.
- Demonstrated Ca(v)1.3 selective coupling to BK channels in membrane nanodomains.
- Showed Ca(v)1.3 and BK channel control of firing frequency and action potential repolarization.
Conclusions:
- Ca(v)1.3 plays a critical role in pacemaker activity.
- The interaction between Ca(v)1.3 and BK channels is vital for regulating neuronal and neuroendocrine cell excitability.
- Understanding this interplay offers insights into physiological processes.
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