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Does ethanol activate G-protein coupled inwardly rectifying K+ channels?
Lih-Chu Chiou1, Kuang-Chieh Chuang, Shu-Huai Fan
1Department of Pharmacology, Medical College, National Taiwan University, Taipei.
Neuroreport
|April 2, 2002
Summary
Ethanol does not affect G-protein coupled inwardly rectifying K+ (GIRK) channels in rat brain regions involved in pain at relevant concentrations. High, lethal ethanol levels activated these channels, suggesting they are not targets for ethanol
Area of Science:
- Neuroscience
- Pharmacology
Background:
- G-protein coupled inwardly rectifying K+ (GIRK) channels are implicated in ethanol's effects.
- The ventrolateral periaqueductal gray (PAG) is crucial for pain regulation.
Purpose of the Study:
- To investigate ethanol's effect on native GIRK channels in the rat ventrolateral PAG at clinically relevant concentrations.
- To determine if GIRK channels in this brain region are targets for ethanol's analgesic effects.
Main Methods:
- Electrophysiological recordings from rat brain slices.
- Application of ethanol at varying concentrations (up to 300 mM).
- Activation of GIRK channels using baclofen, mu-opioid, and nociceptin in unresponsive neurons.
Main Results:
- Ethanol did not affect GIRK currents at concentrations up to 150 mM.
- Ethanol activated barium-sensitive GIRK currents at high, lethal concentrations (200-300 mM) in 30-57% of neurons.
- Baclofen, mu-opioid, and nociceptin activated GIRK channels in ethanol-unresponsive neurons.
Conclusions:
- GIRK channels in the ventrolateral PAG are unlikely targets for the analgesic effects of ethanol.
- Ethanol's effects on GIRK channels require concentrations exceeding therapeutic levels.