van Praag H M
Adv Biochem Psychopharmacol. 1984;39:301-14.
For a long time, antidepressants have been considered to act via enhancement of central MA-ergic activity (due to reuptake or MAO inhibition). An alternative hypothesis holds that their action is based on down-regulation of MA-ergic activity (due to decrease in density or sensitivity of certain receptor populations). In this chapter I have discussed the likelihood of both hypotheses and have reached the conclusion that the first one is the more plausible. I have discussed the following arguments: The 5-HT precursor 5-HTP, which is transformed to 5-HT in the brain, has antidepressant properties. There are indications that the same holds true for tyrosine, a CA precursor transformed in the brain to DA and NE. I found evidence that the 5-HTP effects in depression are potentiated by tyrosine. Since activation rather than suppression of MA-ergic activity seems to be linked to antidepressant activity, it seems likely that the signs of decreased MA metabolism that has been demonstrated in certain types of depression are the expression of a primary metabolic deficit rather than a phenomenon secondary to receptor hyper-sensitivity. Further clinical studies of 5-HT/CA precursor combinations in depression are justified.
长期以来，抗抑郁药一直被认为是通过增强中枢单胺能活性（由于再摄取或单胺氧化酶抑制）来发挥作用的。另一种假说认为，它们的作用基于单胺能活性的下调（由于某些受体群体的密度或敏感性降低）。在本章中，我讨论了这两种假说的可能性，并得出结论，第一种假说更合理。我讨论了以下论点：5-羟色胺前体5-羟色胺酸（5-HTP）在大脑中转化为5-羟色胺（5-HT），具有抗抑郁特性。有迹象表明，对于酪氨酸（一种在大脑中转化为多巴胺（DA）和去甲肾上腺素（NE）的儿茶酚胺前体）来说也是如此。我发现有证据表明，酪氨酸可增强5-羟色胺酸对抑郁症的疗效。由于单胺能活性的激活而非抑制似乎与抗抑郁活性有关，所以在某些类型的抑郁症中所表现出的单胺代谢降低迹象，似乎更有可能是原发性代谢缺陷的表现，而非受体超敏反应继发的现象。因此，有必要对抑郁症患者使用5-羟色胺/儿茶酚胺前体组合进行进一步的临床研究。
