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Two distinct gating mechanisms in gap junction channels: CO2-sensitive and voltage-sensitive
1Department of Pharmacology and Physiology, University of Rochester, School of Medicine and Dentistry, New York 14642-8642, USA.
Biophysical Journal
|May 1, 1997
Summary
Carbon dioxide (CO2) selectively gates gap junction channels through a slow mechanism, influencing channel transitions between open and closed states. This gating impacts channel conductance and kinetics, distinct from voltage-dependent fast flickering.
Area of Science:
- Cellular Biology
- Biophysics
- Neuroscience
Background:
- Gap junction channels mediate direct cell-to-cell communication.
- Connexin43 (Cx43) is a key protein forming gap junctions.
- Chemicals like CO2 can modulate gap junction channel function.
Purpose of the Study:
- To investigate the chemical gating of single gap junction channels by CO2.
- To differentiate the effects of CO2 from voltage-dependent gating.
- To elucidate the kinetic properties of CO2-induced channel gating.
Main Methods:
- Dual whole-cell voltage-clamp recordings in HeLa43 cells and sciatic nerve fibroblasts.
- Analysis of junctional current (Ij), single-channel conductance, and Ij kinetics.
- Application of CO2 for uncoupling and recoupling experiments at varying transjunctional voltages (Vj).
Main Results:
- CO2 induced slow transitions (approx. 10 ms) between open and closed states in the absence of Vj gating (single-channel conductance ~120 pS).
- At high Vj, CO2 also induced slow transitions between residual and closed states, while fast flickering (approx. 2 ms) was voltage-dependent and not clearly linked to CO2.
- During recoupling, channels reopened via slow transitions, followed by fast flickering.
Conclusions:
- Gap junction channels possess distinct slow and fast gating mechanisms.
- CO2 exclusively activates the slow gating mechanism of gap junction channels.
- The findings support a dual gating model for connexin-based channels.