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Influence of escitalopram treatment on 5-HT1A receptor binding in limbic regions in patients with anxiety disorders

Molecular Psychiatry volume 14, pages 1040–1050 (2009)Cite this article

Abstract

There is an increasing interest in the underlying mechanisms of the antidepressant and anxiolytic treatment effect associated with changes in serotonergic neurotransmission after treatment with selective serotonin (5-HT) reuptake inhibitors (SSRIs) in humans. The 5-HT1A receptor is known to play a crucial role in the pathophysiology of affective disorders, and altered 5-HT1A receptor binding has been found in anxiety patients. SSRI treatment raises the 5-HT level in the synaptic cleft and might change postsynaptic receptor densities. Therefore, our study in patients suffering from anxiety disorders investigated the effects of long-term treatment with escitalopram on the 5-HT1A receptor. A longitudinal positrone emission tomography (PET) study in 12 patients suffering from anxiety disorders was conducted. Two dynamic PET scans were performed applying the selective 5-HT1A receptor antagonist [carbonyl-11C]WAY-100635. Eight regions of interest were defined a priori (orbitofrontal cortex, amygdala, hippocampus, subgenual cortex, anterior and posterior cingulate cortex, dorsal raphe nucleus and cerebellum as reference). After the baseline PET scan, patients were administered escitalopram (average dose of 11.2±6.0 mg day−1) for a minimum of 12 weeks. A second PET scan was conducted after 109±27 days. 5-HT1A receptor binding potentials in 12 patients were assessed by PET applying the Simplified Reference Tissue Model.There was a significant reduction in the 5-HT1A receptor binding potential after a minimum of 12 weeks of escitalopram treatment in the hippocampus (P=0.006), subgenual cortex (P=0.017) and posterior cingulate cortex (P=0.034). The significance of the hippocampus region survived the Bonferroni-adjusted threshold for multiple comparisons. These PET data in humans in vivo demonstrate a reduction of the 5-HT1A binding potential after SSRI treatment.

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Acknowledgements

This work was supported by an unrestricted investigator-initiated research grant from H Lundbeck A/S. We are grateful to C Windischberger, E Moser, A Becherer, A Erfurth, N Praschak-Rieder, M Willeit, J Kanaan, N Klein, T Geiss-Granadia, D Ettlinger, T Attarbaschi, S Friedreich and R Dudczak for their scientific, medical or administrative support.

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  1. C Spindelegger and R Lanzenberger: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Psychiatry and Psychotherapy, Medical University Vienna, Vienna, Austria

    C Spindelegger, R Lanzenberger, P Stein, U Moser, A Holik, L Pezawas & S Kasper

  2. Department of Nuclear Medicine, Medical University Vienna, Vienna, Austria

    W Wadsak, L K Mien, M Mitterhauser & K Kletter

  3. Department of Inorganic Chemistry, University of Vienna, Vienna, Austria

    W Wadsak

  4. Department of Pharmaceutical Technology, University of Vienna, Vienna, Austria

    L K Mien & M Mitterhauser

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  1. C Spindelegger
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Correspondence to S Kasper.

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Conflict of interest

S Kasper has received grant/research support from Eli Lilly, Lundbeck, Bristol-Myers Squibb, Servier, Sepracor, GlaxoSmithKline, Organon, has served as a consultant or on advisory boards for AstraZeneca, Austrian Sick Found, Bristol-Myers Squibb, GlaxoSmithKline, Eli Lily, Lundbeck, Pfizer, Organon, Sepracor, Janssen, and Novartis, and has served on speakers’ bureaus for AstraZeneca, Eli Lilly, Lundbeck, Servier, Sepracor and Janssen. K Kletter has received several grants from the pharmaceutical industry in the area of nuclear medicine. L Pezawas, C Spindelegger, R Lanzenberger, U Moser, W Wadsak and M Mitterhauser received travel grants from several companies in CNS research.

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Spindelegger, C., Lanzenberger, R., Wadsak, W. et al. Influence of escitalopram treatment on 5-HT1A receptor binding in limbic regions in patients with anxiety disorders. Mol Psychiatry 14, 1040–1050 (2009). https://doi.org/10.1038/mp.2008.35

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