A new brain mitochondrial sodium-sensitive potassium channel: effect of sodium ions on respiratory chain activity

Author:

Fahanik-babaei Javad12ORCID,Rezaee Bahareh2ORCID,Nazari Maryam3ORCID,Torabi Nihad3ORCID,Saghiri Reza4,Sauve Remy5,Eliassi Afsaneh23ORCID

Affiliation:

1. Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical sciences, Tehran, Iran

2. Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

3. Department of physiology, Shahid Beheshti University of Medical Sciences, Tehran, Iran

4. Department of Biochemistry, Pasteur institute of Iran, Tehran, Iran

5. Department of Pharmacology and Physiology and Membrane Protein Research Group, Université de Montréal, Montréal, Québec H3C 3J7, Canada

Abstract

We have determined the electropharmacological properties of a new potassium channel from brain mitochondrial membrane by planar lipid bilayer method. Our results showed the presence of a channel with a conductance of 150 pS at potentials between 0 and −60 mV in 200 cis/50 trans mM KCl solutions. The channel was voltage-independent, with an open probability value ∼0.6 at different voltages. ATP did not affect current amplitude and Po at positive and negative voltages. Notably, adding iberiotoxin, charybdotoxin, lidocaine, and margatoxin had no effect on the channel behavior. Similarly, no changes were observed by decreasing the cis-pH to 6. Interestingly, the channel was inhibited by adding sodium in a dose dependent manner. Our results also indicated a significant increase in mitochondrial complex IV activity and membrane potential and decrease in complex I activity and mitochondrial ROS production in the presence of sodium ions. We propose that inhibition of mitochondrial K+ transport by Na ions on K+ channel opening may be important for cell protection and ATP synthesis.

Funder

Shahid Beheshti University of Medical Sciences

Publisher

The Company of Biologists

Subject

Cell Biology

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