No change in [11C]CUMI-101 binding to 5-HT1A receptors after intravenous citalopram in human
Version of Record online: 20 JUL 2012
Copyright © 2012 Wiley Periodicals, Inc.
Volume 66, Issue 10, pages 880–884, October 2012
How to Cite
Pinborg, L. H., Feng, L., Haahr, M. E., Gillings, N., Dyssegaard, A., Madsen, J., Svarer, C., Yndgaard, S., Kjaer, T. W., Parsey, R. V., Hansen, H. D., Ettrup, A., Paulson, O. B. and Knudsen, G. M. (2012), No change in [11C]CUMI-101 binding to 5-HT1A receptors after intravenous citalopram in human. Synapse, 66: 880–884. doi: 10.1002/syn.21579
- Issue online: 6 AUG 2012
- Version of Record online: 20 JUL 2012
- Accepted manuscript online: 23 JUN 2012 02:01AM EST
- Manuscript Accepted: 13 JUN 2012
- Manuscript Revised: 5 JUN 2012
- Manuscript Received: 16 MAY 2012
- Lundbeck Foundation
- Danish Council for Independent Research I Humanities
The main objective of this study was to determine the sensitivity of [11C]CUMI-101 to citalopram challenge aiming at increasing extracellular 5-HT. CUMI-101 has agonistic properties in human embryonic kidney 293 cells transfected with human recombinant 5-HT1A receptors (Hendry et al.  Nucl Med Biol 38:273–277; Kumar et al.  J Med Chem 49:125–134) and has previously been demonstrated to be sensitive to bolus citalopram in monkeys (Milak et al.  J Cereb Blood Flow Metab 31:243–249). We studied six healthy individuals. Two PET-scans were performed on the same day in each individual before and after constant infusion of citalopram (0.15 mg/kg). The imaging data were analyzed using two tissue compartment kinetic modeling with metabolite corrected arterial input and Simplified Reference Tissue Modeling using cerebellum as a reference region. There was no significant difference in regional distribution volume or non-displaceable binding potential values before and after citalopram infusion. The mean receptor occupancy was 0.03 (range −0.14 to 0.17). Our data imply that [11C]CUMI-101 binding is not sensitive to citalopram infusion in humans. Synapse, 2012. © 2012 Wiley Periodicals, Inc.