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Benzodiazepine receptor binding in Huntington's disease: [ 11 C]Flumazenil uptake measured using positron emission tomography
Author(s) -
Künig Gabriella,
Leenders Klaus L.,
SanchezPernaute Rosario,
Antonini Angelo,
Vontobel Peter,
Verhagen Aalt,
Günther Ilonka
Publication year - 2000
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(200005)47:5<644::aid-ana13>3.0.co;2-c
Subject(s) - flumazenil , raclopride , benzodiazepine , putamen , positron emission tomography , medicine , binding potential , inverse agonist , brain positron emission tomography , receptor , endocrinology , neuroscience , antagonist , psychology , nuclear medicine , biology , preclinical imaging , genetics , in vivo
Abstract We used positron emission tomography and [ 11 C]flumazenil to analyze the benzodiazepine receptor binding in symptomatic and asymptomatic carriers of the Huntington's disease gene. We found an inverse relationship between [ 11 C]flumazenil and [ 11 C]raclopride binding in the putamen of symptomatic patients, and interpret this result as GABA receptor upregulation. We used positron emission tomography and [ 11 C]flumazenil to analyze the benzodiazepine receptor binding in symptomatic and asymptomatic carriers of the Huntington's disease gene. We found an inverse relationship between [ 11 C]flumazenil and [ 11 C]raclopride binding in the putamen of symptomatic patients, and interpret this result as GABA receptor upregulation. Ann Neurol 2000;47:644–648