脑源性神经营养因子在抑郁症发生和治疗中的研究进展  

Research development of brain-derived neurotrophic factor in the occur and treatment of depression

作　　者：张扬[1] 董文心[1] 

机构地区：[1]上海医药工业研究院

出　　处：《世界临床药物》2008年第10期623-627,共5页World Clinical Drug

摘　　要：目前临床常用的抗抑郁药主要通过增加脑内突触间隙单胺类递质的浓度、增强单胺类神经的功能而起效,但这一机制不能很好地解释抗抑郁药存在的起效时间长等现象。近年提出,抗抑郁药可能还通过增加海马区域脑源性神经营养因子(BDNF)基因表达起效。抗抑郁药能增加受试动物海马区BDNF基因表达,抑郁患者接受抗抑郁药治疗,其血清BDNF水平上升;BDNF基因的单核苷酸多态性也与抑郁症的发生有关;抗抑郁药可能还通过激活丝裂原活化蛋白激酶(MAPK)信号通路,磷酸化cAMP反应序列结合(CREB)蛋白,最终使BDNF基因表达上调。这一机制的提出为抑郁症生物学病因的阐明提供了必要信息,同时也有助于抗抑郁新药的开发,为研制安全、有效的新药提供新的思路。Now the antidepressants used in clinic produced the effects mainly through increasing the monoamines in synaptic cleft of brain, thereby enhanced the monoaminergic neuron function. But this theory disagreed with the phe- nomenon of antidepressants＇ effect delay. Recently, new theory suggested that antidepressants may effect by increasing the brain-derived neurotrophic factor （BDNF） expression in hippocampus. Firstly, antidepressants may up-regulate BDNF expression in animals, and increase plasma BDNF level in patients after antidepressants treatment. Secondly, BDNF gene polymorphism related to depression. Thirdly, antidepressants may activate mitogen-activated protein kinase （MAPK） signal pathway, then phosphorylate cAMP response element-binding （CREB） protein, and finally increase BDNF expression. This theory may provide the evidence for pathogeny of depression. In another hand, it will help the development of new antidepressants, and provide a new ideal to develop much more safe and effective antidepressants.

关 键 词：抗抑郁药 作用机制 脑源性神经营养因子 

分 类 号：R749.41[医药卫生—神经病学与精神病学]