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Schizophrenia Bulletin Advance Access published online on June 12, 2009
Schizophrenia Bulletin, doi:10.1093/schbul/sbp010
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© The Author 2009. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Presynaptic Regulation of Dopamine Transmission in Schizophrenia

Gholson J. Lyon2,8, Anissa Abi-Dargham2,5, Holly Moore2,6, Jeffrey A. Lieberman2,7, Jonathan A. Javitch2,4,7,9 and David Sulzer14,9
2 Department of Psychiatry
3 Department of Neurology
4 Department of Pharmacology, Columbia University, New York, NY
5 Division of Translational Imaging
6 Division of Integrative Neuroscience
7 Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, NY
8 Present address: Department of Child and Adolescent Psychiatry, NYU Child Study Center, New York, NY
9 These authors contributed equally to this work

1 To whom correspondence should be addressed; Department of Neurology, Columbia University, Black 309, 650 W 168th Street, New York City, NY 10032; tel: 212-305-3967, fax: 212-305-5450, e-mail: ds43{at}columbia.edu.

A role for dopamine (DA) release in the hallucinations and other positive symptoms associated with schizophrenia has long been inferred from the antipsychotic response to D2 DA receptor antagonists and because the DA releaser amphetamine can be psychotogenic. Recent studies suggest that patients with schizophrenia, including those never exposed to antipsychotic drugs, maintain high presynaptic DA accumulation in the striatum. New laboratory approaches are elucidating mechanisms that control the level of presynaptic DA stores, thus contributing to fundamental understanding of the basic pathophysiologic mechanism in schizophrenia.

Keywords: dopamine / positron emission tomography / vesicular monoamine transporter / aromatic amine decarboxylase / raclopride / F-DOPA / animal models / schizophrenia


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