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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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Published in: | British journal of psychiatry 1998-08, Vol.173 (2), p.116-122 |
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container_title | British journal of psychiatry |
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creator | 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. |
description | 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. |
doi_str_mv | 10.1192/bjp.173.2.116 |
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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.</description><identifier>ISSN: 0007-1250</identifier><identifier>EISSN: 1472-1465</identifier><identifier>DOI: 10.1192/bjp.173.2.116</identifier><identifier>PMID: 9850223</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Adult ; Alcohol ; Alcoholism ; Alcoholism - diagnostic imaging ; Alcoholism - metabolism ; Alcoholism - pathology ; Atrophy ; Benzodiazepine receptors ; Benzodiazepines ; Brain ; Brain - diagnostic imaging ; Brain - metabolism ; Brain - pathology ; Cerebral cortex ; Dependency ; Emissions ; Gamma-aminobutyric acid ; Humans ; Magnetic resonance imaging ; Magnetic Resonance Imaging - methods ; Male ; Multiple regression analysis ; Neurotransmitters ; Parietal lobe ; Photon emission tomography ; Questionnaires ; Receptors, GABA-A - metabolism ; Regression analysis ; Single photon emission computed tomography ; Single photon emission tomography ; Statistical analysis ; Substantia grisea ; Tomography ; Tomography, Emission-Computed, Single-Photon - methods ; γ-Aminobutyric acid</subject><ispartof>British journal of psychiatry, 1998-08, Vol.173 (2), p.116-122</ispartof><rights>Copyright © 1998 The Royal College of Psychiatrists</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c477t-eba1129c383b1a77e438703d46d60c9639ea57fac97bfe5e52e55662841866f23</citedby><cites>FETCH-LOGICAL-c477t-eba1129c383b1a77e438703d46d60c9639ea57fac97bfe5e52e55662841866f23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0007125000150925/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>315,786,790,12873,27957,27958,31034,73317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9850223$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lingford-Hughes, Anne R.</creatorcontrib><creatorcontrib>Acton, P.</creatorcontrib><creatorcontrib>Gacinovic, S.</creatorcontrib><creatorcontrib>Suckling, J.</creatorcontrib><creatorcontrib>Busatto, G. F.</creatorcontrib><creatorcontrib>Boddington, S. J. A.</creatorcontrib><creatorcontrib>Bullmore, E.</creatorcontrib><creatorcontrib>Woodruff, P. W.</creatorcontrib><creatorcontrib>Costa, D. C.</creatorcontrib><creatorcontrib>Pilowsky, L. S.</creatorcontrib><creatorcontrib>Ell, P. J.</creatorcontrib><creatorcontrib>Marshall, E. J.</creatorcontrib><creatorcontrib>Kerwin, R. W.</creatorcontrib><title>Reduced levels of GABA-benzodiazepine receptor in alcohol dependency in the absence of grey matter atrophy</title><title>British journal of psychiatry</title><addtitle>Br J Psychiatry</addtitle><description>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.</description><subject>Adult</subject><subject>Alcohol</subject><subject>Alcoholism</subject><subject>Alcoholism - diagnostic imaging</subject><subject>Alcoholism - metabolism</subject><subject>Alcoholism - pathology</subject><subject>Atrophy</subject><subject>Benzodiazepine receptors</subject><subject>Benzodiazepines</subject><subject>Brain</subject><subject>Brain - diagnostic imaging</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Cerebral cortex</subject><subject>Dependency</subject><subject>Emissions</subject><subject>Gamma-aminobutyric acid</subject><subject>Humans</subject><subject>Magnetic resonance imaging</subject><subject>Magnetic Resonance Imaging - methods</subject><subject>Male</subject><subject>Multiple regression analysis</subject><subject>Neurotransmitters</subject><subject>Parietal lobe</subject><subject>Photon emission tomography</subject><subject>Questionnaires</subject><subject>Receptors, GABA-A - metabolism</subject><subject>Regression analysis</subject><subject>Single photon emission computed tomography</subject><subject>Single photon emission tomography</subject><subject>Statistical analysis</subject><subject>Substantia grisea</subject><subject>Tomography</subject><subject>Tomography, Emission-Computed, Single-Photon - methods</subject><subject>γ-Aminobutyric acid</subject><issn>0007-1250</issn><issn>1472-1465</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>7QJ</sourceid><sourceid>ALSLI</sourceid><sourceid>HEHIP</sourceid><sourceid>M2R</sourceid><recordid>eNptkEtLxDAUhYMoOj6WLoWI6455tEm7HAdfIAii65Amt9MOnaYmHaX-ejPMoAiuLufej3MuB6FzSqaUFuy6XPZTKvmURSn20ISmkiU0Fdk-mhBCZEJZRo7QcQjLKHnK5CE6LPKMMMYnaPkCdm3A4hY-oA3YVfh-djNLSui-nG30F_RNB9iDgX5wHjcd1q1xtWuxhR46C50ZN9uhBqzLECVsTBYeRrzSwwAe68G7vh5P0UGl2wBnu3mC3u5uX-cPydPz_eN89pSYVMohgVJTygrDc15SLSWkPJeE21RYQUwheAE6k5U2hSwryCBjkGVCsDyluRAV4yfoauvbe_e-hjCopVv7LkYqxvOCy0iKSCVbyngXgodK9b5ZaT8qStSmWBWLVbFYxaLc8Bc713W5AvtD75qM98vtvW4W9WfjQXnTh9HUfzyud5l6VfrGLuD3tf9TvwHMS45X</recordid><startdate>19980801</startdate><enddate>19980801</enddate><creator>Lingford-Hughes, Anne R.</creator><creator>Acton, P.</creator><creator>Gacinovic, S.</creator><creator>Suckling, J.</creator><creator>Busatto, G. F.</creator><creator>Boddington, S. J. A.</creator><creator>Bullmore, E.</creator><creator>Woodruff, P. W.</creator><creator>Costa, D. C.</creator><creator>Pilowsky, L. S.</creator><creator>Ell, P. J.</creator><creator>Marshall, E. J.</creator><creator>Kerwin, R. 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F. ; Boddington, S. J. A. ; Bullmore, E. ; Woodruff, P. W. ; Costa, D. C. ; Pilowsky, L. S. ; Ell, P. J. ; Marshall, E. J. ; Kerwin, R. 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F.</creatorcontrib><creatorcontrib>Boddington, S. J. A.</creatorcontrib><creatorcontrib>Bullmore, E.</creatorcontrib><creatorcontrib>Woodruff, P. W.</creatorcontrib><creatorcontrib>Costa, D. C.</creatorcontrib><creatorcontrib>Pilowsky, L. S.</creatorcontrib><creatorcontrib>Ell, P. J.</creatorcontrib><creatorcontrib>Marshall, E. J.</creatorcontrib><creatorcontrib>Kerwin, R. 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F.</au><au>Boddington, S. J. A.</au><au>Bullmore, E.</au><au>Woodruff, P. W.</au><au>Costa, D. C.</au><au>Pilowsky, L. S.</au><au>Ell, P. J.</au><au>Marshall, E. J.</au><au>Kerwin, R. W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced levels of GABA-benzodiazepine receptor in alcohol dependency in the absence of grey matter atrophy</atitle><jtitle>British journal of psychiatry</jtitle><addtitle>Br J Psychiatry</addtitle><date>1998-08-01</date><risdate>1998</risdate><volume>173</volume><issue>2</issue><spage>116</spage><epage>122</epage><pages>116-122</pages><issn>0007-1250</issn><eissn>1472-1465</eissn><abstract>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.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>9850223</pmid><doi>10.1192/bjp.173.2.116</doi><tpages>7</tpages></addata></record> |
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subjects | Adult Alcohol Alcoholism Alcoholism - diagnostic imaging Alcoholism - metabolism Alcoholism - pathology Atrophy Benzodiazepine receptors Benzodiazepines Brain Brain - diagnostic imaging Brain - metabolism Brain - pathology Cerebral cortex Dependency Emissions Gamma-aminobutyric acid Humans Magnetic resonance imaging Magnetic Resonance Imaging - methods Male Multiple regression analysis Neurotransmitters Parietal lobe Photon emission tomography Questionnaires Receptors, GABA-A - metabolism Regression analysis Single photon emission computed tomography Single photon emission tomography Statistical analysis Substantia grisea Tomography Tomography, Emission-Computed, Single-Photon - methods γ-Aminobutyric acid |
title | Reduced levels of GABA-benzodiazepine receptor in alcohol dependency in the absence of grey matter atrophy |
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