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Updated: Apr 4, 2026
15:28
Mutagenesis and Functional Analysis of Ion Channels Heterologously Expressed in Mammalian Cells
Published on: October 1, 2010
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Ethanol Effect on BK Channels is Modulated by Magnesium
Héctor G Marrero1, Steven N Treistman1, José R Lemos2
1Institute of Neurobiology UPR-MSC, San Juan, Puerto Rico.
Alcoholism, Clinical and Experimental Research
|September 3, 2015
Summary
Ethanol (EtOH) affects calcium-dependent potassium channels (BK) differently based on intracellular magnesium (Mg2+) levels. This interaction, particularly involving actin, may explain molecular tolerance in chronic alcohol drinkers.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Alcoholism is associated with reduced intracellular magnesium (Mg2+).
- Calcium-dependent potassium channels (BK) are molecular targets of ethanol (EtOH).
Purpose of the Study:
- To investigate how intracellular Mg2+ concentration modulates EtOH's effects on BK channels.
Main Methods:
- Utilized outside-out patches from hippocampal neuronal cultures and HEK cells expressing BK channels.
- Examined the influence of varying intracellular Mg2+ concentrations on EtOH-induced BK channel activity.
- Assessed the role of actin interactions using cytochalasin D and phalloidin.
Main Results:
- EtOH's effect on BK channels is bimodal, dependent on intracellular Mg2+ concentration.
- At low Mg2+ (≤200 μM), EtOH inhibits BK activity; at high Mg2+ (1 mM), EtOH potentiates activity.
- Actin interactions modulate EtOH's effect, with stabilization leading to inhibition and destabilization to Mg2+-independence.
Conclusions:
- Intracellular Mg2+ modulates EtOH's action on BK channels via actin interactions at the synapse.
- A decrease in cytoplasmic Mg2+ in chronic drinkers may lead to reduced EtOH effects on synaptic BK channels, contributing to molecular tolerance.
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