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Reduced levels of GABA-benzodiazepine receptor in alcohol dependency in the absence of grey matter atrophy

We tested the hypothesis that reduced levels of the GABA-benzodiazepine receptor occur in alcohol dependency using single photon emission tomography (SPET) and the specific GABA-benzodiazepine ligand, 123I-iomazenil. Neurologically and cognitively unimpaired abstinent alcohol-dependent (n = 12) and...

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Bibliographic Details
Published in:British journal of psychiatry 1998-08, Vol.173 (2), p.116-122
Main Authors: Lingford-Hughes, Anne R., Acton, P., Gacinovic, S., Suckling, J., Busatto, G. F., Boddington, S. J. A., Bullmore, E., Woodruff, P. W., Costa, D. C., Pilowsky, L. S., Ell, P. J., Marshall, E. J., Kerwin, R. W.
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Language:English
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Summary:We tested the hypothesis that reduced levels of the GABA-benzodiazepine receptor occur in alcohol dependency using single photon emission tomography (SPET) and the specific GABA-benzodiazepine ligand, 123I-iomazenil. Neurologically and cognitively unimpaired abstinent alcohol-dependent (n = 12) and non-alcohol-dependent male subject (n = 14) underwent a 123I-iomazenil SPET scan. SPET and magnetic resonance images were co-registered and voxel-based statistical tests performed. Subjects' clinical and alcohol history were obtained with standard questionnaires. The relationships between clinical and alcohol variables and the regional level of GABA-benzodiazepine receptors were investigated using multiple regression analysis. Abstinent alcohol-dependent subjects had decreased levels of GABA-benzodiazepine receptor compared with non-alcohol-dependent subjects within the frontal, parietal and temporal cortices, including regions in which grey matter atrophy was absent. Alcohol dependency is associated with reduced GABA-benzodiazepine receptor levels in the absence of grey matter atrophy in some cortical regions, such as within the parietal lobe. Regional variability of reduction in GABA-benzodiazepine receptors demonstrates that alcohol does not have a global, toxic effect on the brain.
ISSN:0007-1250
1472-1465
DOI:10.1192/bjp.173.2.116