Waldmeier P C
Eur J Pharmacol. 1979 Dec 20;60(4):315-22. doi: 10.1016/0014-2999(79)90235-8.
The potentiation of the effect of haloperidol on rat striatal homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) by a serotonin (5-HT) uptake inhibitor, CGP 6085 A, has been further investigated. The evidence that this effect of CGP 6085 A is related to its 5-HT uptake inhibitory properties is discussed. The potentiation was antagonized by scopolamine and baclofen, and disappeared more rapidly than the uptake inhibitory effects of CGP 6085 A, presumably because the effects of uptake inhibition were counteracted by a reduction in 5-HT synthesis. CGP 6085 A also potentiated the effects of fluphenazine and pimozide, but not those of a number of other neuroleptics. It also failed to restore the effect of haloperidol in animals treated chronically with the neuroleptic. These results appear to indicate that CGP 6085 A can only stimulate DA neurons if their activity is already above the resting level. The antagonism of this effect by scopolamine suggests that the site of action of the 5-HT uptake inhibitor is before a cholinergic neuron.
已对5-羟色胺（5-HT）摄取抑制剂CGP 6085 A增强氟哌啶醇对大鼠纹状体高香草酸（HVA）和3,4-二羟基苯乙酸（DOPAC）作用的现象作了进一步研究。文中讨论了CGP 6085 A的这一作用与其5-HT摄取抑制特性相关的证据。东莨菪碱和巴氯芬可拮抗这种增强作用，且该增强作用比CGP 6085 A的摄取抑制作用消失得更快，推测是因为5-HT合成减少抵消了摄取抑制的作用。CGP 6085 A还增强了氟奋乃静和匹莫齐特的作用，但对其他多种抗精神病药物则无此作用。它也不能恢复长期接受抗精神病药物治疗的动物体内氟哌啶醇的作用。这些结果似乎表明，只有当多巴胺（DA）神经元的活性已高于静息水平时，CGP 6085 A才能刺激它们。东莨菪碱对这一作用的拮抗表明，5-HT摄取抑制剂的作用位点在胆碱能神经元之前。
