Lindholm Jesse S O, Castrén Eero
Neuroscience Center, University of Helsinki Helsinki, Finland.
Front Behav Neurosci. 2014 Apr 30;8:143. doi: 10.3389/fnbeh.2014.00143. eCollection 2014.
Brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase TrkB support neuronal survival during development and promote connectivity and plasticity in the adult brain. Decreased BDNF signaling is associated with the pathophysiology of depression and the mechanisms underlying the actions of antidepressant drugs (AD). Several transgenic mouse models with decreases or increases in the amount of BDNF or the activity of TrkB signaling have been created. This review summarizes the studies where various mouse models with increased or decreased BDNF levels or TrkB signaling were used to evaluate the role of BDNF signaling in depression-like behavior. Although a large number of models have been employed and several studies have been published, no clear-cut connections between BDNF levels or signaling and depression-like behavior in mice have emerged. However, it is clear that BDNF plays a critical role in the mechanisms underlying the actions of AD.
脑源性神经营养因子(BDNF)及其受体酪氨酸激酶TrkB在发育过程中支持神经元存活,并促进成人大脑中的连接性和可塑性。BDNF信号通路的减弱与抑郁症的病理生理学以及抗抑郁药物(AD)作用的潜在机制有关。已经创建了几种BDNF量或TrkB信号活性降低或增加的转基因小鼠模型。本综述总结了使用各种BDNF水平或TrkB信号增加或减少的小鼠模型来评估BDNF信号在抑郁样行为中的作用的研究。尽管已经采用了大量模型并发表了几项研究,但小鼠中BDNF水平或信号与抑郁样行为之间尚未出现明确的联系。然而,很明显BDNF在AD作用的潜在机制中起着关键作用。