首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >DYNAMIC PLASTICITY: THE ROLE OF GLUCOCORTICOIDS, BRAIN-DERIVED NEUROTROPHIC FACTOR AND OTHER TROPHIC FACTORS
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DYNAMIC PLASTICITY: THE ROLE OF GLUCOCORTICOIDS, BRAIN-DERIVED NEUROTROPHIC FACTOR AND OTHER TROPHIC FACTORS

机译:动态可塑性:糖皮质激素,脑源性神经营养因子和其他营养因子的作用

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Brain-derived neurotrophic factor (BDNF) is a secreted protein that has been linked to numerous aspects of plasticity in the central nervous system (CNS). Stress-induced remodeling of the hippocampus, prefrontal cortex and amygdala is coincident with changes in the levels of BDNF, which has been shown to act as a trophic factor facilitating the survival of existing and newly born neurons. Initially, hippocampal atrophy after chronic stress was associated with reduced BDNF, leading to the hypothesis that stress-related learning deficits resulted from suppressed hippocampal neurogenesis. However, recent evidence suggests that BDNF also plays a rapid and essential role in regulating synaptic plasticity, providing another mechanism through which BDNF can modulate learning and memory after a stressful event. Numerous reports have shown BDNF levels are highly dynamic in response to stress, and not only vary across brain regions but also fluctuate rapidly, both immediately after a stressor and over the course of a chronic stress paradigm. Yet, BDNF alone is not sufficient to effect many of the changes observed after stress. Glucocorticoids and other molecules have been shown to act in conjunction with BDNF to facilitate both the morphological and molecular changes that occur, particularly changes in spine density and gene expression. This review briefly summarizes the evidence supporting BDNF's role as a trophic factor modulating neuronal survival, and will primarily focus on the interactions between BDNF and other systems within the brain to facilitate synaptic plasticity. This growing body of evidence suggests a more nuanced role for BDNF in stress-related learning and memory, where it acts primarily as a facilitator of plasticity and is dependent upon the coactivation of glucocorticoids and other factors as the determinants of the final cellular response.
机译:脑源性神经营养因子(BDNF)是一种分泌蛋白,已与中枢神经系统(CNS)可塑性的许多方面相关。应激诱导的海马,前额叶皮层和杏仁核的重塑与BDNF水平的变化相吻合,这已被证明是促进现有和新生神经元存活的营养因子。最初,慢性应激后海马萎缩与BDNF降低有关,从而导致假说,与应激相关的学习缺陷是由抑制海马神经发生引起的。但是,最近的证据表明,BDNF在调节突触可塑性中也起着快速而必不可少的作用,它提供了另一种机制,BDNF可以通过这种机制在压力事件后调节学习和记忆。许多报告表明,BDNF水平在应对压力时具有很高的动态性,不仅在大脑区域变化,而且在压力源之后和在慢性压力范式中均迅速波动。然而,仅BDNF不足以实现压力后观察到的许多变化。糖皮质激素和其他分子已显示与BDNF协同作用,以促进发生的形态和分子变化,特别是脊柱密度和基因表达的变化。这篇综述简要总结了支持BDNF作为调节神经元存活的营养因子的作用的证据,并将主要关注BDNF和大脑其他系统之间的相互作用,以促进突触可塑性。越来越多的证据表明,BDNF在与压力有关的学习和记忆中起着更细微的作用,它主要起可塑性的促进作用,并依赖于糖皮质激素和其他因素的共激活作为最终细胞反应的决定因素。

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