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Subanesthetic ketamine does not affect 11C-flumazenil binding in humans
Elina Salmi1, Jaakko W Långsjö, Sargo Aalto
1Turku PET Centre, Centre for Cognitive Neuroscience, and the Department of Pharmacology and Clinical Pharmacology, University of Turku, and the Departments of Anesthesiology and Intensive Care, Child Neurology, and Psychiatry, Turku University Hospital, Turku, Finland; Institute of Biomedicine, Pharmacology, University of Helsinki, Helsinki, Finland.
Abstract:
Positron emission tomography (PET) studies suggest that propofol and inhaled anesthetics increase (11)C-flumazenil binding in the living human brain, thus supporting the involvement of gamma-aminobutyric acid type A (GABA(A)) receptors in the mechanism of action of these drugs. Ketamine produces its anesthetic effects primarily by N-methyl-d-aspartate receptor antagonism, but it may also have GABA(A) receptor agonistic properties. By using PET, we studied the cerebral (11)C-flumazenil binding in 10 healthy subjects before and during a subanesthetic racemic ketamine infusion reaching a serum concentration of 350 +/- 42 ng/mL. Ketamine did not affect (11)C-flumazenil binding to GABA(A) receptor in the brain, indicating that this mechanism is of minor importance in the actions of subanesthetic ketamine.
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