Mousseau D D
Neuroscience Research Unit, André-Viallet Clinical Research Center, Hôpital St-Luc (University of Montréal), Québec, Canada.
Metab Brain Dis. 1993 Mar;8(1):1-44. doi: 10.1007/BF01000528.
Although early interest in the biomedical relevance of tryptamine has waned in recent years, it is clear from the above discussion that the study of tryptamine is worthy of serious consideration as a factor in neuropsychiatric disorders. The study of [3H]-tryptamine binding sites indicates an adaptive responsiveness characteristic of functional receptors. The question raised by Jones (1982d) on whether tryptamine is acting centrally as a neurotransmitter or a neuromodulator still remains mostly unanswered, although the evidence cited within this review strongly suggests a modulatory role for this neuroactive amine (see also Juorio and Paterson, 1990). The synthesis and degradative pathways of tryptamine, as well as the intricate neurochemical and behavioral consequences of altering these pathways, are now more fully understood. It is not yet clear what the role of tryptamine is under normal physiological [homeostatic] conditions, however, its role during pathological conditions such as mental and physical stress, hepatic dysfunction and other disorders of metabolism (i.e. electrolyte imbalance, increased precursor availability, enzyme induction or alterations in enzyme co-factor availability) may be quite subtle, perhaps accounting for various sequelae hitherto considered idiopathic. The evidence for a primary role for tryptamine in the etiology of mental or neurological diseases is still relatively poor, although the observations that endogenous concentrations of tryptamine are particularly susceptible to pharmacological as well as physiological manipulations serve to reinforce the proposition that this indoleamine is not simply a metabolic accident but rather a neuroactive compound in its own right. Finally, one might wonder what proportion of the data attributed to modifications of 5-HT metabolism might, in fact, involve unrecognized changes in the concentrations of other neuroactive metabolites of tryptophan such as tryptamine.
尽管近年来对色胺生物医学相关性的早期兴趣有所减弱，但从上述讨论中可以清楚地看出，色胺研究作为神经精神疾病的一个因素值得认真考虑。对[3H] - 色胺结合位点的研究表明了功能性受体的适应性反应特征。琼斯（1982d）提出的关于色胺在中枢是作为神经递质还是神经调质起作用的问题，尽管本综述中引用的证据强烈表明这种神经活性胺具有调节作用（另见朱里奥和帕特森，1990），但大多仍未得到解答。色胺的合成和降解途径，以及改变这些途径所产生的复杂神经化学和行为后果，现在已经得到了更充分的理解。然而，色胺在正常生理[稳态]条件下的作用尚不清楚，其在诸如精神和身体应激、肝功能障碍以及其他代谢紊乱（即电解质失衡、前体可用性增加、酶诱导或酶辅因子可用性改变）等病理条件下的作用可能相当微妙，也许可以解释迄今为止被认为是特发性的各种后遗症。色胺在精神或神经疾病病因学中起主要作用的证据仍然相对不足，尽管观察到色胺的内源性浓度特别容易受到药理学以及生理学操作的影响，这进一步支持了这样一种观点，即这种吲哚胺不仅仅是一种代谢产物，而是一种本身就具有神经活性的化合物。最后，人们可能会想，事实上，归因于5 - 羟色胺代谢改变的数据中，有多大比例可能涉及色氨酸其他神经活性代谢产物（如色胺）浓度未被认识到的变化。
