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Inactivation of the ERG current in NG108-15 cells.

¹I. Physiologisches, Institut der Universität des Saarlandes, Homburg-Saar, D-66421, Germany.

Biochemical and Biophysical Research Communications

|September 24, 1999

Summary

The inactivation rate of ether-à-go-go related gene (ERG) potassium channels slows as external potassium concentration decreases. This finding is crucial for understanding ERG channel function in varying physiological conditions.

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Area of Science:

Neuroscience
Molecular Biology
Biophysics

Background:

The ether-à-go-go related gene (ERG) potassium channel is vital for cardiac repolarization and neuronal excitability.
Understanding the factors influencing ERG channel gating, particularly inactivation, is essential for comprehending its physiological roles.

Purpose of the Study:

To investigate the effect of extracellular potassium concentration ([K+](o)) on the inactivation kinetics of ERG potassium channels.
To characterize the relationship between membrane potential and ERG channel inactivation time constants under different [K+](o) conditions.

Main Methods:

Whole-cell voltage clamp electrophysiology was performed on differentiated NG108-15 neuroblastoma x glioma hybrid cells.
A three-pulse voltage protocol was employed to measure ERG channel inactivation rates.
The selective ERG channel blocker E-4031 was used to isolate ERG currents and avoid contamination from delayed rectifier currents.

Main Results:

The inactivation time constant (tau) of ERG channels was dependent on both membrane potential and extracellular potassium concentration.
Lowering [K+](o) significantly decreased the tau of inactivation across tested potentials.
At -20 mV, tau decreased from 25.4 ms in 40 mM K+ to 15.0 ms in 0 mM K+.
The relationship between tau and membrane potential could be described by a Gaussian curve, with the peak shifting at different [K+](o).

Conclusions:

Extracellular potassium concentration is a critical determinant of ERG potassium channel inactivation kinetics.
The observed dependence of ERG channel inactivation on [K+](o) in NG108-15 cells mirrors findings in other expression systems, suggesting conserved mechanisms.
These findings contribute to a better understanding of ERG channel function in physiological and pathological states characterized by altered extracellular potassium levels.

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