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- Title
Ketamine does not decrease striatal dopamine D[sub 2] receptor binding in man.
- Authors
Aalto, Sargo; Hirvonen, Jussi; Kajander, Jaana; Scheinin, Harry; Någren, Kjell; Vilkman, Harry; Gustafsson, Lars; Syvälahti, Erkka; Hietala, Jarmo
- Abstract
Rationale: A glutamate-dopamine interaction has been implicated in the psychosis-like effects of glutamate N-methyl-D-aspartate (NMDA) receptor antagonists, such as phencyclidine and ketamine. However, recent imaging studies addressing striatal glutamatedopamine interaction directly in vivo in man have been controversial. Objectives: To examine whether the NMDA receptor antagonist ketamine in high subanesthetic concentrations decreases striatal [[sup 11]C]raclopride binding potential in man. To further evaluate whether changes in striatal [[sup 11]C]raclopride binding are associated with ketamine-induced behavioral effects. Methods: The effect of computer-driven subanesthetic ketamine infusion on striatal dopamine release was studied in healthy male subjects using a controlled study design. Dopamine release was studied using positron emission tomography and the [[sup 11]C]raclopride displacement paradigm. A conventional region of interest-based analysis and voxelbased analysis were applied to the positron emission tomography data. Results: The average plasma ketamine concentration was 293±29 ng/ml. Ketamine did not alter striatal [[sup 11]C]raclopride binding. Ketamine induced typical behavioral effects, such as hallucinations but there was no correlation between these effects and displacement of [[sup 11]C]raclopride binding. Conclusions: This controlled study indicates that ketamine does not decrease striatal [[sup 11]C]raclopride binding. Striatal dopamine release is of minor importance in the psychosis-like effects of ketamine.
- Subjects
KETAMINE; DOPAMINE receptors
- Publication
Psychopharmacology, 2002, Vol 164, Issue 4, p401
- ISSN
0033-3158
- Publication type
Article
- DOI
10.1007/s00213-002-1236-6