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Effect of Diazepam on Plasma γ‐Aminobutyric Acid in Sons of Alcoholic Fathers
Author(s) -
Cowley Deborah S.,
RoyByrne Peter P.,
Greenblatt David J.,
Kramer Gerald L.,
Petty Frederick
Publication year - 1996
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.1530-0277.1996.tb01650.x
Subject(s) - diazepam , gamma aminobutyric acid , psychology , sedative , medicine , pharmacology , placebo , agonist , novelty seeking , endocrinology , aminobutyric acid , receptor , personality , big five personality traits , alternative medicine , pathology , social psychology
A subgroup of abstinent alcoholics display low levels of plasma γ‐aminobutyric acid (GABA). Two previous studies of plasma GABA in sons of alcoholic fathers (SOAs) have yielded conflicting results. The aim of the current study was to measure plasma GABA both at baseline and after challenge with diazepam, a GABA A receptor agonist, in a group of SOAs already shown to display decreased eye movement, memory, and sedative effects of diazepam. Twenty‐seven SOAs and 23 male control subjects received four logarithmically increasing doses of diazepam or placebo in randomized order on 2 days at least 1 week apart. Plasma GABA was measured at baseline and after the last dose. There were no significant differences between SOAs and controls in baseline plasma GABA levels. In the whole sample, there were significant correlations between baseline plasma GABA and both high novelty‐seeking and low‐harm avoidance scores on the Tridimensional Personality Questionnaire. Both SOAs and controls displayed decreases in plasma GABA over time on both testing days, but there was no effect of diazepam on plasma GABA and no significant difference between groups in plasma GABA response to diazepam. These results suggest that neither low plasma GABA at baseline nor altered plasma GABA response to diazepam is associated with increased genetic risk for alcoholism.