Bookmark this page

Reduction of cortical 5-HT2A receptor binding in drug-naive but not in paroxetine-responder depressed patients
Many studies have suggested that 5-HT2A receptors are involved in the pathophysiology of depression and that an association may exist between clinical improvement and binding to these receptors. Changes in their density have, however, yielded conflicting results. Among the factors which may contribute to these discrepancies is the absence of a direct comparison between depressed subjects and healthy controls. A study was thus designed to compare 5-HT2A receptor binding between patients with major depressive disorder (MDD), either never treated with antidepressants (drug-naive, DN) or responding to the selective serotonin reuptake inhibitor, paroxetine (drug-treated, DT), and healthy volunteers.
Among 34 patients diagnosed with MDD, 19 had never been treated with any antidepressant drug and 15 were in their 4th week of treatment with paroxetine. These subjects were compared with a group of 20 heathy controls. Positron emission tomography (PET) with [18F]fluoroethylspiperone ([18F]FESP), a 5-HT2A receptor antagonist and dopamine D2 receptor antagonist, was used and a binding index (BI) of [18F]FESP to cortical (serotonergic) and striatal (dopaminergic) regions was calculated as the ratio of binding in these regions compared to that of cerebellum (considered to represent background "noise".
Binding was reduced in naive patients in the frontal, occipital, temporal and cingulate cortices, but not in the striatum. BI values of the whole cortex of these these subjects were reduced by 23% compared to those of normal controls. No differences were found between treated patients and healthy controls.
These results lend support to a relationship between depressive symptoms and the decrease of 5-HT2A receptor binding. In addition a return to normal binding value would explain the unaltered binding value in patients responding to paroxetine. [18F]FESP binding to cortical regions may be useful to detect state-related changes in depression and therefore represent a depression marker.
Psychopharmacology 167: 72-78, 2003

Disclaimer

Site conceived and produced by NeuroBiz Consulting & Communications
© Depression-WebWorld Ltd UK, 2003