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Is [11c]cumi-101 binding to 5-ht1a receptors susceptible to intravenous citalopram challenge in humans?
IS [11C]CUMI-101 BINDING TO 5-HT1A RECEPTORS SUSCEPTIBLE TO INTRAVENOUS
CITALOPRAM CHALLENGE IN HUMANS?
1,2,3, L. Feng1, M. Haahr1, N. Gillings4, A. Ettrup1, H.D. Hansen1, S. Yndgaard5, C.
Svarer1, G.M. Knudsen1,3
1Neurobiology Research Unit, N9201, 2Epilepsy Clinic, N8501, 3The Lundbeck Centre for Integrated Molecular Brain Imaging, 4The PET & Cyclotron Unit, 5Department of Thoratic Anaesthesiology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
Introduction and hypothesis:
We previously failed to demonstrate a translation of intravenous
citalopram challenge into a change in 5-HT2A binding of [18F]altanserin binding(1). Whether we
consider changes in radioligand binding following pharmacological challenges to be the result of
simple competition between radioligand and 5-HT or the result of agonist-mediated receptor
internalization, the fact that most of the 5-HT2A receptors are located intracellularly and
[18F]altanserin is an antagonist radioligand are likely to be the most important explanations.
Here we present our preliminary results in three healthy subjects using citalopram challenge
and the new 5-HT1A agonist radioligand [11C]CUMI-101. Our hypothesis is that [11C]CUMI-101
binding to 5-HT1A receptors is reduced following acute citalopram challenge. Methods:
[11C]CUMI-101was synthesized as previously described(2). [11C]CUMI-101was
injected as a bolus and PET (high-resolution research tomography scanner, Siemens AG) data
were subsequently collected for 120 minutes. Arterial blood samples were obtained during PET
scanning and metabolite corrected using HPLC as previously described(3). Thirty minutes after
ending the first PET experiment one hour of constant Citalopram (H. Lundbeck A/S, 0.15 mg kg-
1) infusion started. Thirty minutes after Citalopram infusion started a second [11C]CUMI-101-PET
experiment was conducted similar to the first experiment. MRI was conducted on a Siemens
Magnetom Trio 3 T MR scanner (Invivo, FL, USA) and co-registred to the PET image. VOIs
were automatically delineated on each individual's MRI in a strictly user-independent fashion(4).
Kinetic modeling (unconstrained 2-tissue compartment modeling and simplified tissue reference
modeling) was done in PMOD (version 3.0). Results:
In subject 3 the final analysis of blood data in the baseline situation is to be completed. Conclusion:
Our preliminary results do not imply a decrease in [11C]CUMI-101 binding to 5-
HT1A receptors following intravenous citalopram challenge. The literature suggests a decrease
in regional cerebral blood flow following intravenous administration of citalopram. Our K1 and R1
values do not imply a quantitatively important reduction in tracer delivery following citalopram
challenge. Our results do not imply that the use of cerebellum as a reference region is
hampered by the increase in extracellular 5-HT following citalopram infusion. Recent
unpublished data (Hendry-N et al.) suggest that [11C]CUMI-101 behaves as an antagonist on
rodent cortical 5-HT1A receptors. Sensitivity of [11C]CUMI-101to acute pharmacological
challenge in monkeys has been demonstrated but at much larger doses of citalopram (2-4 mg
kg-1)(5). Thus, the challenge paradigm and the radiotracer may not be optimal for measuring
acute changes in extracellular 5-HT. Further studies are needed to draw more firm conclusions
using this experimental set-up. References:
(1) Pinborg et al. (2004) J Cereb Blood Flow Metab
(2) Kumar et al. (2007) Eur J Nucl Med Mol Imaging
34:1050-60 (3) Gillings-N (2009) Nucl Med Biol
36:961-65 (4) Svarer et al. (2005) Neuroimage
24:969-79 (5) Milak et al. (2010) J Cereb Blood Flow Metab
: Epub ahead of print
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