Moeller F G, Steinberg J L, Fulton M, Kramer G, Petty F
Department of Psychiatry and Behavioral Sciences, University of Texas Houston Health Science Center 77030.
Neuropsychopharmacology. 1994 Apr;10(2):75-83. doi: 10.1038/npp.1994.9.
We administered the serotonin-1a agonist buspirone (0.4 mg/kg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III-R major depressive disorder (MDD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between 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 prolactin level than nonmelancholic depressed patients (n = 8). Our findings support a role for the serotonin-1a receptor in the etiology of MDD, specifically at the postsynaptic site.
我们给一组患有DSM-III-R重度抑郁症（MDD）的男性患者（n = 13）和一组男性健康对照者（n = 10）口服血清素-1a激动剂丁螺环酮（0.4毫克/千克），作为一种神经内分泌激发剂。该研究的主要假设是，抑郁症患者对丁螺环酮的催乳素反应会减弱。抑郁症患者的催乳素反应显著低于对照组。安慰剂校正后的催乳素峰值水平与抑郁严重程度或自杀倾向之间没有显著关系。 melancholic（n = 5）抑郁症患者的安慰剂校正后的催乳素峰值水平有低于非melancholic抑郁症患者（n = 8）的趋势，但不显著。我们的研究结果支持血清素-1a受体在MDD病因学中的作用，特别是在突触后位点。
