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Keywords:

  • Hyperbaric Exposure;
  • Ethanol Antagonist;
  • GABAA;
  • Receptor;
  • LS Microsacs

Previous studies have shown that exposure to 12 times normal atmospheric pressure of helium-oxygen gas (heliox) directly antagonizes a range of ethanol's acute and chronic behavioral effects. The present study extends the investigation to the biochemical level by investigating the effects of pressure on ethanol-induced potentiation of GABAA receptor function in mouse membrane vesicles (micro-sacs). Exposure to 12 atmospheric pressure heliox significantly antagonized ethanol (25 to 100 mM) potentiation of GABA-activated 36Cl- uptake, but did not significantly alter baseline GABAA receptor function measured by the response of the system to GABA (10 to 100 μM), bicuculline (3 and 100 μM), or picrotoxin (100 μM). These findings add essential support for the hypothesis that hyperbaric exposure is a direct ethanol antagonist that can be used as a tool to help identify ethanol's initial cellular and molecular sites of action that cause its behavioral effects. Taken in context with previous behavioral studies, the present results also provide important new evidence for a cause-effect relationship between ethanol potentiation of GABAA receptor function and ethanol's anesthetic and behavioral effects.