The Interplay between Brain-Derived Neurotrophic Factors and Stress Hormone Modulates the Process of Neurogenesis

Brain-derived neurotrophic factor (BDNF) is molecule that enhances the growth and maintenance of neurons in the central nervous system [1,2]. BDNF is highly expressed in the hippocampal and cortical regions of the brain where they involved in neuronal survival, synaptic plasticity and the formation of long-lasting memories [3-5]. Their high affinity receptor, TrkB has been identified as the Trk family of tyrosine protein kinases, thus facilitate to understand the signaling pathways responsible for mediating their trophic properties [6]. TrkB receptor is phosphorylated by binding of BDNF that trigger the activation of ERK-, Akt-, and PLC gamma-pathways [7-9]. Each pathway contributes to multifarious neuronal functions, including neurogenesis and the regulation of cell fate [10,11]. Various studies demonstrated that reduced expression of BDNF along with depressive behaviors, suggesting that an alteration in status of the BDNF/TrkB system leads to reduction in neurogenesis resulting brain dysfunctioning. Chronic stress reduces mRNA levels of BDNF [10,12] is one of the most important endogenous mediators of stress responses in the mammalian brain. Glucocorticoids (GCs) a stress hormone, exert influence on neurogenesis and functions, as well as BDNF [13]. Blood levels of GCs are regulated by hypothalamus-pituitaryadrenal (HPA) axis activity [14-16]. It is well known that chronic stress induces the hyper activation of HPA axis, resulting overabundance of GCs levels [16]. Elevated levels of GCs have a role in the onset of mental disorders, including post-traumatic stress disorder, major depressive disorders and neurodegeneration. Furthermore, GC stress suppress the formation of neuron synthesis, especially in hippocampal region, has been a vulnerable target to develop new drugs because it shows the dysregulation of HPA axis function [17,18] and is considered as a culprit that leads to the onset of the mental disorders [19]. This review article demonstrated the functional interaction between BDNF and GCs towards altered neurogenesis.