脑源性神经营养因子(brain derived neurotrophic factor,BDNF)是一个关键性的神经营养因子,它既影响突触的形成和重构,又可以通过突触前和突触后机制改变突触传递的效能,从而对神经结构和功能可塑性发挥调节作用。BDNF主要通过结合TrkB受体激活细胞内信号系统来发挥它积极的生物学效应。研究表明,中枢神经系统BDNF表达或功能的变化与抑郁症的发生相关,而应激引起糖皮质激素(glucocorticoid,GC)的增加也是导致抑郁发生的重要原因之一。值得注意的是,GCs的增加会影响BDNF,一方面GCs降低BDNF的表达,另一方面GCs受体GR与BNDF受体TrkB相互作用。过多的GCs干扰了BDNF信号,使BDNF功能受到影响,导致抑郁患者脑内,尤其是海马结构的损害。就抑郁发生中糖皮质激素对BDNF功能影响的研究进展作一介绍。
Brain-derived neurotrophic factor (BDNF) is a critical neurotrophin in the formation and reconstruction of synapses, and alters the synaptic transmission efficiency by regulating pre- and post-synaptic mechanisms, which in turn leads to the adjustment of neural structural and functional plasticity. Combined with neurons via activation of TrkB and intracellular signaling, BDNF could exert its biological effects positively. Studies have shown that the change of BDNF expression and function is associated with depression, and the elevation of glucocorticoids (GCs) is also involved in the pathophysiology of depression. Notably, the increase of GCs can reduce the level of BDNF, and the glucocorticoid receptor also can interact with TrkB, a receptor of BDNF. BDNF signal will be interfered with the excessive glucocorticoids, which will alter the functions of BDNF, and lead to the hippocampus damage at last. This review discusses the effect of GCs on BDNF in the development of stress-induced depression.