The “serotonin hypothesis” of depression proposes that a diminished serotonergic (5-HT)
neurotransmission is causal in the pathophysiology of the disorder. Although over
50 years old, there is no firm in vivo evidence for diminished 5-HT neurotransmission.
We have recently demonstrated that the 5-HT2A receptor (5-HR2A-R) agonist PET radioligand,
[11C]Cimbi-36, is sensitive to increases in extracellular 5-HT induced by an acute
d-amphetamine challenge (1). Here we applied [11C]Cimbi-36 PET to compare brain 5-HT
release capacity (SRC) in patients undergoing a major depressive episode (MDE) to
that of non-depressed healthy controls (HC).
