Journal
BIOLOGICAL PSYCHIATRY
Volume 71, Issue 3, Pages 239-246Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2011.06.026
Keywords
(1)H-MRS; alcohol; brain; GABA; glutamate; NAA
Categories
Funding
- National Institutes of Health [P50 AA12870, R01 DA021785, R21 AA018210, 2R01AA011321, KO5 AA 14906, K02 MH076222]
- Clinical and Translational Science Award [UL1 RR024139]
- Department of Veterans Affairs (VA) via the VA Alcohol Research Center
- State of Connecticut
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico of Brazil
- Dana Foundation
- AstraZeneca
- Bristol-Myers Squibb
- Hoffman La-Roche
- Merck and Company
- Sepracor (Sunovion)
- Medtronic
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Background: Ethanol modulates glutamate and gamma-aminobutyric (GABA) function. However, little is known about the acute pharmacologic effects of ethanol on levels of GABA, glutamate, and other metabolites measurable in the human cortex in vivo with proton magnetic resonance spectroscopy ((1)H-MRS). Methods: Eleven healthy social drinkers received two intravenous ethanol infusions that raised breath alcohol levels to a clamped plateau of 60 mg/dL over 60-70 min. The first infusion established tolerability of the procedure, and the second procedure, conducted 15 +/- 12 days later, was performed during (1)H-MRS of occipital GABA, glutamate, and other metabolites. Results: The time course of brain ethanol approximated that of breath ethanol, but venous ethanol lagged by approximately 7 min. The GABA fell 13 +/- 8% after 5 min of the ethanol infusion and remained reduced (p = .003) throughout the measurement. The combination of N-acetylaspartate and N-acetylaspartyl glutamate (summed as NAA) fell steadily during the infusion by 8 +/- 3% (p = .0036). Conclusions: Ethanol reduced cortical GABA and NAA levels in humans. Reductions in GABA levels are consistent with facilitation of GABA(A) receptor function by ethanol. The gradual decline in NAA levels suggests inhibition of neural or metabolic activity in the brain.
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