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Intracellular Mg(2+) enhances the function of BK-type Ca(2+)-activated K(+) channels.

Shi J, Cui J - J. Gen. Physiol. (2001)

Bottom Line: Intracellular Mg(2+) also modulates BK channels in multiple ways with opposite effects on channel function.We have confirmed this result by studying macroscopic currents of the mslo1 channel.Quantitative computation of these effects reveals that the overall effect of Mg(2+) under physiological conditions is to enhance BK channel function.

View Article: PubMed Central - PubMed

Affiliation: Cardiac Bioelectricity Research and Training Center, Case Western Reserve University, Cleveland, OH 44106-7207, USA.

ABSTRACT
BK channels modulate neurotransmitter release due to their activation by voltage and Ca(2+). Intracellular Mg(2+) also modulates BK channels in multiple ways with opposite effects on channel function. Previous single-channel studies have shown that Mg(2+) blocks the pore of BK channels in a voltage-dependent manner. We have confirmed this result by studying macroscopic currents of the mslo1 channel. We find that Mg(2+) activates mslo1 BK channels independently of Ca(2+) and voltage by preferentially binding to their open conformation. The mslo3 channel, which lacks Ca(2+) binding sites in the tail, is not activated by Mg(2+). However, coexpression of the mslo1 core and mslo3 tail produces channels with Mg(2+) sensitivity similar to mslo1 channels, indicating that Mg(2+) sites differ from Ca(2+) sites. We discovered that Mg(2+) also binds to Ca(2+) sites and competitively inhibits Ca(2+)-dependent activation. Quantitative computation of these effects reveals that the overall effect of Mg(2+) under physiological conditions is to enhance BK channel function.

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Intracellular Mg(2+) enhances the function of BK-type Ca(2+)-activated K(+) channels.

Shi J, Cui J - J. Gen. Physiol. (2001)

© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2233844&req=5

Bottom Line: Intracellular Mg(2+) also modulates BK channels in multiple ways with opposite effects on channel function.We have confirmed this result by studying macroscopic currents of the mslo1 channel.Quantitative computation of these effects reveals that the overall effect of Mg(2+) under physiological conditions is to enhance BK channel function.

View Article: PubMed Central - PubMed

Affiliation: Cardiac Bioelectricity Research and Training Center, Case Western Reserve University, Cleveland, OH 44106-7207, USA.

ABSTRACT
BK channels modulate neurotransmitter release due to their activation by voltage and Ca(2+). Intracellular Mg(2+) also modulates BK channels in multiple ways with opposite effects on channel function. Previous single-channel studies have shown that Mg(2+) blocks the pore of BK channels in a voltage-dependent manner. We have confirmed this result by studying macroscopic currents of the mslo1 channel. We find that Mg(2+) activates mslo1 BK channels independently of Ca(2+) and voltage by preferentially binding to their open conformation. The mslo3 channel, which lacks Ca(2+) binding sites in the tail, is not activated by Mg(2+). However, coexpression of the mslo1 core and mslo3 tail produces channels with Mg(2+) sensitivity similar to mslo1 channels, indicating that Mg(2+) sites differ from Ca(2+) sites. We discovered that Mg(2+) also binds to Ca(2+) sites and competitively inhibits Ca(2+)-dependent activation. Quantitative computation of these effects reveals that the overall effect of Mg(2+) under physiological conditions is to enhance BK channel function.

Show MeSH