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Social Cognitive and Affective Neuroscience Advance Access first published online on November 16, 2008
This version published online on January 20, 2009
Social Cognitive and Affective Neuroscience, doi:10.1093/scan/nsn039
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© The Author (2009). Published by Oxford University Press. For Permissions, please email: journals.permissions@oxfordjournals.org

Reduced 5-HT2A receptor signaling following selective bilateral amygdala damage

René Hurlemann1,2,*, Thomas E. Schlaepfer2,3,*, Andreas Matusch4, Harald Reich2, Nadim J. Shah4,5, Karl Zilles1,5,6, Wolfgang Maier1,2 and Andreas Bauer1,4,7

1Brain Imaging Center West, Research Center Juelich, 52425 Juelich, Germany, 2Department of Psychiatry, University of Bonn, 53105 Bonn, Germany, 3Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University, Baltimore, MD 21287-7413, USA, 4Institute of Neuroscience and Biophysics 3 – Medicine, Research Center Juelich, 52425 Juelich, Germany, 5Institute of Physics, University of Dortmund, 44221 Dortmund, Germany, 6C. & O. Vogt Institute for Brain Research and 7Department of Neurology, University of Duesseldorf, 40225 Duesseldorf, Germany

Neurobiological evidence implicates the amygdala as well as serotonergic (serotonin, 5-HT) signaling via postsynaptic 5-HT2A receptors as essential substrates of anxiety behaviors. Assuming a functional interdependence of these substrates, we hypothesized that a low-fear behavioral phenotype due to bilateral lesion of the amygdala would be associated with significant 5-HT2A receptor changes. Thus, we used [18F]altanserin positron emission tomography (PET) referenced to radioligand plasma levels and corrected for partial volume effects to quantify the spatial distribution of 5-HT2A receptor binding potential (BPP) in a rare patient with Urbach–Wiethe disease and selective bilateral amygdala calcification damage relative to 10 healthy control subjects. Consistent with our a priori hypothesis, we observed a 70% global decrease in 5-HT2A receptor BPP in the Urbach–Wiethe patient relative to controls. Thus, brain abnormalities in this patient are not restricted to the amygdala, but extend to overall 5-HT neurotransmission via 5-HT2A receptors. Our findings provide important insights into the molecular architecture of human anxiety behaviors and suggest the 5-HT2A receptor as a promising pharmacological target to control pathological anxiety.

Keywords: Amygdala; fear; anxiety; serotonin; 5-HT2A receptor; PET; Urbach-Wiethe disease

Correspondence should be addressed to René Hurlemann, M.Sc., M.D., Ph.D., Department of Psychiatry, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. E-mail: renehurlemann{at}me.com

*These authors contributed equally to this work.

Received June 4, 2008. Accepted October 9, 2008.


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