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HIGHER IN VIVO SEROTONIN‐1A BINDING IN POSTTRAUMATIC STRESS DISORDER: A PET STUDY WITH [ 11 C]WAY‐100635
Author(s) -
Sullivan Gregory M.,
Ogden R. Todd,
Huang Yungyu,
Oquendo Maria A.,
Mann J. John,
Parsey Ramin V.
Publication year - 2013
Publication title -
depression and anxiety
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.634
H-Index - 129
eISSN - 1520-6394
pISSN - 1091-4269
DOI - 10.1002/da.22019
Subject(s) - 5 ht1a receptor , binding potential , major depressive disorder , serotonin , medicine , psychology , raphe nuclei , endocrinology , amygdala , neuroscience , serotonergic , oncology , 5 ht receptor , positron emission tomography , receptor
Background Brain serotonin‐1A receptors (5‐HT 1A ) are implicated in anxiety. We compared regional brain 5‐HT 1A binding in medication‐free participants with posttraumatic stress disorder (PTSD) and healthy volunteers using fully quantitative positron emission tomography (PET) methods. Methods Twenty patients with DSM‐IV PTSD (13 with comorbid major depressive disorder, [MDD]) and 49 healthy volunteers underwent PET imaging with 5‐HT 1A antagonist radioligand [C‐11]WAY100635. Arterial blood sampling provided a metabolite‐corrected input function and the concentration of free ligand in plasma (f P ) for estimation of regional binding potential, BP F ( = B available / K D ). Linear mixed modeling compared BP F between groups across regions of interest (ROIs). Results The PTSD group had higher 5‐HT 1A BP F across brain ROIs (P = .0006). Post hoc comparisons showed higher 5‐HT 1A BP F in PTSD in all cortical ROIs (26–33%), amygdala (34%), and brainstem raphe nuclei (43%), but not hippocampus. The subgroup of seven PTSD patients without comorbid MDD had higher 5‐HT 1A BP F compared with healthy volunteers (P = .03). Conclusions This is the first report of higher brainstem and forebrain 5‐HT 1A binding in vivo in PTSD. The finding is independent of MDD. PTSD and MDD have in common an upregulation of 5‐HT 1A binding including midbrain autoreceptors that would favor less firing and serotonin release. This abnormality may represent a common biomarker of these stress‐associated brain disorders.