Ketamine does not decrease striatal dopamine D2 receptor binding in man
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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 glutamate–dopamine interaction directly in vivo in man have been controversial.
Objectives. To examine whether the NMDA receptor antagonist ketamine in high subanesthetic concentrations decreases striatal [11C]raclopride binding potential in man. To further evaluate whether changes in striatal [11C]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 [11C]raclopride displacement paradigm. A conventional region of interest-based analysis and voxel-based 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 [11C]raclopride binding. Ketamine induced typical behavioral effects, such as hallucinations but there was no correlation between these effects and displacement of [11C]raclopride binding.
Conclusions. This controlled study indicates that ketamine does not decrease striatal [11C]raclopride binding. Striatal dopamine release is of minor importance in the psychosis-like effects of ketamine.
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