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Low‐Level Hyperbaric Antagonism of Ethanol‐Induced Locomotor Depression in C57BL/6J Mice: Dose Response
Author(s) -
Bejanian M.,
Jones B. L.,
Alkana R. L.
Publication year - 1993
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1993.tb05644.x
Subject(s) - antagonism , depression (economics) , ethanol , pharmacology , medicine , endocrinology , chemistry , biochemistry , receptor , economics , macroeconomics
This study characterized the antagonistic effects of hyperbaric exposure on the dose‐response curve for ethanol‐induced depression of locomotor activity. Drug‐naive, male C57BL/6 mice were injected intraperitoneally with saline, 1.5, 2.0, 2.5, or 3.0 g/kg ethanol, and were exposed to 1 atmosphere absolute (ATA) air or 12 ATA helium‐oxygen gas mixtures (heliox) at temperatures that offset the hypothermic effects of ethanol and helium. Locomotor activity was measured 10‐30 min after injection. In addition, the effects of exposure to 12 ATA heliox on blood ethanol concentrations were tested in a separate group of mice injected with 2.5 g/kg ethanol. Ethanol produced a dose‐dependent depression of locomotor activity beginning at 2.0 g/kg. Exposure to 12 ATA heliox completely antagonized the locomotor depressant effects of 2.0 and 2.5 g/kg ethanol and partially blocked the effects of 3.0 g/kg. Activity in mice given 1.5 g/ kg ethanol was not significantly affected at 1 ATA air, but was significantly increased at 12 ATA heliox. Low‐level hyperbaric exposure shifted the ethanol dose‐response curve to the right with a resultant increase in the ED 50 of ethanol for locomotor depression from 2.6 to 3.3 g/kg. Exposure to 12 ATA heliox did not alter blood ethanol concentrations in mice injected with 2.5 g/kg ethanol. These findings with 12 ATA heliox present key new evidence for the hypothesis that low‐level hyperbaric exposure acts directly, with a pattern analogous to a competitive, mechanistic antagonist of ethanol.