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Quantification of Striatal Dopamine Transporters with ¹²³I-FP-CIT SPECT Is Influenced by the Selective Serotonin Reuptake Inhibitor Paroxetine: A Double-Blind, Placebo-Controlled, Crossover Study in Healthy Control Subjects

¹ Department of Nuclear Medicine, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; ² Graduate School for Neurosciences, Amsterdam, The Netherlands; and ³ Department of Radiology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands

Correspondence: For correspondence or reprints contact: Jan Booij, MD, Department of Nuclear Medicine, F2N, University of Amsterdam, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam The Netherlands. E-mail: J.Booij{at}amc.uva.nl

Dopamine transporter (DAT) imaging with ¹²³I-FP-CIT (¹²³I-N--fluoropropyl-2ß-carbomethoxy-3ß-(4-iodophenyl)nortropane) SPECT is frequently used to detect loss of nigrostriatal cells in parkinsonism. Recent ¹²³I-ß-CIT (¹²³I-2ß-carbomethoxy-3ß-(4-iodophenyl)tropane) studies have shown a significant increase in striatal-to-nonspecific ß-CIT binding ratios after treatment with selective serotonin reuptake inhibitors (SSRIs). Due to similarities between ¹²³I-ß-CIT and ¹²³I-FP-CIT (both are derived from cocaine and show relatively high affinity for the DAT and the serotonin transporter [SERT]), we hypothesized that quantification of striatal ¹²³I-FP-CIT binding may be influenced by SSRIs. Moreover, we hypothesized that ¹²³I-FP-CIT in humans binds not only to DATs but also to central and peripheral SERTs. Methods: To study the influence of the SSRI paroxetine on ¹²³I-FP-CIT binding to DATs in the striatum, we conducted a double-blind, placebo-controlled, crossover study with paroxetine in 8 healthy young male control subjects. In addition, we studied whether paroxetine was able to block ¹²³I-FP-CIT binding in SERT-rich brain areas and in lung tissue, as lung tissue contains a considerable amount of SERTs. Participants were pretreated for 2 d with paroxetine (20 mg/d) or placebo at 2 sessions (crossover design), and brain SPECT was performed 1 and 3 h after ¹²³I-FP-CIT injection, whereas lung uptake was measured 2 h after injection. Results: Compared with placebo pretreatment, we found after paroxetine pretreatment a statistically significant increase (approximately 10%) in specific striatal-to-nonspecific ¹²³I-FP-CIT binding ratios at 3 h after injection, a time point at which striatal ¹²³I-FP-CIT binding ratios are stable. In addition, after paroxetine treatment, statistically significantly lower binding ratios were found in SERT-rich brain areas (e.g., at 1 h after injection, midbrain-to-cerebellar ratios were approximately 90% lower) as well as significantly lower uptake in lung tissue was found (approximately 40% lower after paroxetine). Conclusion: In this study we show that the quantification of striatal ¹²³I-FP-CIT binding to DAT is significantly increased by the SSRI paroxetine in humans. To our knowledge, this is the first study which shows that ¹²³I-FP-CIT binds in vivo in humans not only to DATs but also to central SERTs and SERTs in lung tissue.

Key Words: FP-CIT SPECT • dopamine transporter • serotonin transporter • paroxetine

COPYRIGHT © 2007 by the Society of Nuclear Medicine, Inc.

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