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The Journal of Neuroscience, October 28, 2009, 29(43):13730-13734; doi:10.1523/JNEUROSCI.4172-09.2009

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Behavioral/Systems/Cognitive
Effects of the Antipsychotic Risperidone on Dopamine Synthesis in Human Brain Measured by Positron Emission Tomography with L-[β-¹¹C]DOPA: A Stabilizing Effect for Dopaminergic Neurotransmission?

Hiroshi Ito, Harumasa Takano, Hidehiko Takahashi, Ryosuke Arakawa, Michie Miyoshi, Fumitoshi Kodaka, Masaki Okumura, Tatsui Otsuka, and Tetsuya Suhara

Clinical Neuroimaging Team, Molecular Neuroimaging Group, Molecular Imaging Center, National Institute of Radiological Sciences, Chiba 263-8555, Japan

Correspondence should be addressed to Dr. Hiroshi Ito, Clinical Neuroimaging Team, Molecular Neuroimaging Group, Molecular Imaging Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan. Email: hito{at}nirs.go.jp

Effects of antipsychotic drugs have widely been considered to be mediated by blockade of postsynaptic dopamine D₂ receptors. Effects of antipsychotics on presynaptic functions of dopaminergic neurotransmission might also be related to therapeutic effects of antipsychotics. To investigate the effects of antipsychotics on presynaptic functions of dopaminergic neurotransmission in relation with occupancy of dopamine D₂ receptors, changes in dopamine synthesis capacity by antipsychotics and occupancy of dopamine D₂ receptors were measured by positron emission tomography (PET) in healthy men. PET studies using [¹¹C]raclopride and L-[β-¹¹C]DOPA were performed under resting condition and oral administration of single dose of the antipsychotic drug risperidone on separate days. Although occupancy of dopamine D₂ receptors corresponding dose of risperidone was observed, the changes in dopamine synthesis capacity by the administration of risperidone were not significant, nor was the relation between the occupancy of dopamine D₂ receptors and these changes. A significant negative correlation was observed between the baseline dopamine synthesis capacity and the changes in dopamine synthesis capacity by risperidone, indicating that this antipsychotic can be assumed to stabilize the dopamine synthesis capacity. The therapeutic effects of risperidone in schizophrenia might be related to such stabilizing effects on dopaminergic neurotransmission responsivity.

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Received Aug. 24, 2009; revised Sept. 26, 2009; accepted Sept. 30, 2009.

Correspondence should be addressed to Dr. Hiroshi Ito, Clinical Neuroimaging Team, Molecular Neuroimaging Group, Molecular Imaging Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan. Email: hito{at}nirs.go.jp

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