Abstract
Altered neurogenesis is suggested to be involved in the onset of brain diseases, including mental disorders and neurodegenerative diseases. Neurotrophic factors are well known for their positive effects on the proliferation/differentiation of both embryonic and adult neural stem/progenitor cells (NSCs/NPCs). Especially, brain-derived neurotrophic factor (BDNF) has been extensively investigated because of its roles in the differentiation/maturation of NSCs/NPCs. On the other hand, recent evidence indicates a negative impact of the stress hormone glucocorticoids (GCs) on the cell fate of NSCs/NPCs, which is also related to the pathophysiology of brain diseases, such as depression and autism spectrum disorder. Furthermore, studies including ours have demonstrated functional interactions between neurotrophic factors and GCs in neural events, including neurogenesis. In this review, we show and discuss relationships among the behaviors of NSCs/NPCs, BDNF, and GCs.
Highlights
Brain-derived neurotrophic factor (BDNF) is highly expressed in the brain, including hippocampal and cortical regions, and has pivotal roles in the maintenance of neurons in the central nervous system (CNS)
It is well established that activation of ERK, Akt, and PLCgamma-pathways are triggered by TrkB phosphorylation induced by binding of BDNF, and each pathway contributes a variety of neuronal functions, including the regulation of cell fate [1,2,3]
Altered neurogenesis under GC stress, especially in hippocampal region, has been an important therapeutic target to develop new drugs because suppression of hippocampal neurogenesis may contribute to the dysregulation of HPA-axis function [12,13] and is considered as one of the causes that leads to the onset of the mental disorders mentioned above
Summary
Brain-derived neurotrophic factor (BDNF) is highly expressed in the brain, including hippocampal and cortical regions, and has pivotal roles in the maintenance of neurons in the central nervous system (CNS). Blood levels of GCs are regulated by hypothalamus-pituitary-adrenal (HPA) axis activity. It is well known that excess and chronic stress causes hyper activation of the HPA axis, which results in abnormally increased levels of GCs [6,7], and such an increased GCs has a role in the onset of mental disorders, including post-traumatic stress disorder and major depressive disorders [8,9,10,11]. Altered neurogenesis under GC stress, especially in hippocampal region, has been an important therapeutic target to develop new drugs because suppression of hippocampal neurogenesis may contribute to the dysregulation of HPA-axis function [12,13] and is considered as one of the causes that leads to the onset of the mental disorders mentioned above. We discuss recent studies concerning functional interaction between BDNF and GCs in altered neurogenesis, and show an interesting effect of GCs: Alteration in intracellular transport of BDNF protein under GC stress
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