Journal
JOURNAL OF NEUROSCIENCE
Volume 29, Issue 43, Pages 13730-13734Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4172-09.2009
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Funding
- Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japanese government
- Japan Society for the Promotion of Science [21591587]
- Grants-in-Aid for Scientific Research [21591587] Funding Source: KAKEN
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Effects of antipsychotic drugs have widely been considered to be mediated by blockade of postsynaptic dopamine D-2 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 D-2 receptors, changes in dopamine synthesis capacity by antipsychotics and occupancy of dopamine D-2 receptors were measured by positron emission tomography (PET) in healthy men. PET studies using [C-11] raclopride and L-[beta-C-11] DOPA were performed under resting condition and oral administration of single dose of the antipsychotic drug risperidone on separate days. Although occupancy of dopamine D-2 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 D-2 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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