RT Journal Article SR Electronic T1 Reduced Serotonin Type 1A Receptor Binding in Panic Disorder JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 589 OP 591 DO 10.1523/JNEUROSCI.4921-03.2004 VO 24 IS 3 A1 Alexander Neumeister A1 Earle Bain A1 Allison C. Nugent A1 Richard E. Carson A1 Omer Bonne A1 David A. Luckenbaugh A1 William Eckelman A1 Peter Herscovitch A1 Dennis S. Charney A1 Wayne C. Drevets YR 2004 UL http://www.jneurosci.org/content/24/3/589.abstract AB Recent animal models suggest that disturbances in serotonin type-1A receptor (5-HT1AR) function may contribute to chronic anxiety, although it is not clear at all whether such models constitute relevant models for panic disorder (PD) in humans. The selective 5-HT1AR radioligand [18F]trans-4-fluoro-N-2-[4-(2-methoxyphenyl)piperazin-1-yl]ethyl]-N-(2-pyridyl)cyclohexanecarboxamide (FCWAY) permits in vivo assessment of central 5-HT1AR binding using positron emission tomography (PET). We studied 16 unmedicated symptomatic outpatients with PD and 15 matched healthy controls. Seven patients had an additional diagnosis of a current major depressive episode, however PD was the primary diagnosis. A 120 min PET study of 5-HT1AR binding was acquired using a GE Advance scanner in three-dimensional mode. Using quantitative PET image analysis, regional values were obtained for [18F]-FCWAY volume of distribution (DV), corrected for plasma protein binding, and K1, the delivery rate of [18F]-FCWAY from plasma to tissue. MRI scanning was performed using a GE Signa Scanner (3.0 Tesla) to provide an anatomical framework for image analysis and partial volume correction of PET data. PD patients showed lower DV in the anterior cingulate (t = 4.3; p < 0.001), posterior cingulate (t = 4.1; p < 0.001), and raphe (t = 3.1; p = 0.004). Comparing patients with PD, patients with PD and comorbid depression, and healthy controls revealed that DVs did not differ between PD patients and PD patients with comorbid depression, whereas both patient groups differed significantly from controls. These results provide for the first time in vivo evidence for the involvement of 5-HT1ARs in the pathophysiology of PD.