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Gating currents in Shaker K+ channels. Implications for activation and inactivation models
E Perozo1, D M Papazian, E Stefani
1Department of Physiology, University of California, Los Angeles 90024.
Biophysical Journal
|April 1, 1992
Summary
Investigating Shaker K+ channels reveals that channel activation is not due to independent subunits. The inactivation particle, not identical subunits, drives charge immobilization during channel gating.
Area of Science:
- Molecular Biology
- Biophysics
- Neuroscience
Background:
- Shaker K+ channels are crucial for neuronal excitability.
- Understanding their gating and inactivation mechanisms is key to ion channel function.
- The relationship between voltage sensors and inactivation particles remains an area of active research.
Purpose of the Study:
- To investigate the mechanisms of Shaker K+ channel activation.
- To explore the link between the channel's voltage sensor and its inactivation particle.
- To elucidate the kinetics of gating currents in wild-type and mutant channels.
Main Methods:
- Studied ionic and gating currents in mutant and wild-type Shaker K+ channels.
- Utilized hyperpolarizing prepulses to analyze voltage-dependence.
- Investigated the effect of internal tetraethylammonium (TEA) on charge immobilization.
Main Results:
- Gating current onset shows a rising phase, suggesting non-independent activation subunits.
- Voltage dependence primarily occurs during transitions between closed states.
- Fast inactivation in Shaker channels leads to partial immobilization of off-gating charge, mimicked and enhanced by internal TEA.
Conclusions:
- Shaker K+ channel activation does not involve identical, independent gating subunits undergoing first-order transitions.
- The inactivation particle is responsible for charge immobilization during channel gating.
- The open-to-closed transition is voltage-independent.