We administered the serotonin-1a agonist buspirone (0.4 mg/kg orally)
as a neuroendocrine challenge agent to a group of maze patients with D
SM-III-R major depressive disorder (MDD) (n = 13) and a group of male
healthy controls (n = 10). The primary hypothesis of the study was tha
t the prolactin response to buspirone would be blunted in the depresse
d patients. The prolactin response was significantly lower in depresse
d patients than in controls. There was no significant relationship bet
ween placebo corrected-peak prolactin level and severity of depression
or suicidality. There was a nonsignificant trend for the melancholic
(n = 5) depressed patients to have a lower placebo corrected-peak prol
actin level than nonmelancholic depressed patients (n = 8). Our findin
gs support a role for the serotonin-la receptor in the etiology of MDD
, specifically at the postsynaptic site.