Cereseto M, Ferrero A
CONICET, Buenos Aires, Argentina.
Vertex. 2003 Mar-May;14(51):30-5.
Depression is a highly prevalent condition in adult population. Research on the mechanism of action of antidepressant drugs is also expected to allow a better comprehension about its etiopathogenesis. First theories about neurobiology of depression pointed out the monoaminergic modifications elicited by antidepressants. However, these changes could not be correlated with the latency of action observed in their clinical use. In 1997, with the formulation of genomic theory of depression, old theories and new knowledge about cellular and molecular effects of antidepressant treatment became congruent. The main goal of this paper is to review this theory and the scientific papers in which it is supported. Scientific evidences against genomic theory of antidepressant action are also mentioned. CREB's participation in antidepressant response, as well as BDNF trophic effect and their intracellular signaling pathways are described, as many of these molecules could become targets for the action of new antidepressants.
抑郁症在成年人群中非常普遍。对抗抑郁药物作用机制的研究也有望使人们更好地理解其病因学。关于抑郁症神经生物学的最初理论指出了抗抑郁药引起的单胺能改变。然而，这些变化与它们在临床使用中观察到的起效潜伏期并无关联。1997年，随着抑郁症基因组理论的提出，关于抗抑郁治疗的细胞和分子效应的旧理论与新知识变得一致。本文的主要目的是回顾这一理论以及支持该理论的科学文献。同时也提及了反对抗抑郁作用基因组理论的科学证据。描述了CREB在抗抑郁反应中的参与情况，以及BDNF的营养作用及其细胞内信号通路，因为这些分子中的许多可能成为新型抗抑郁药作用的靶点。
