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Signaling mechanisms linking neuronal activity to gene expression and plasticity of the nervous system.
Annual Review of Neuroscience ( IF 12.1 ) Pub Date : 2008-01-01 , DOI: 10.1146/annurev.neuro.31.060407.125631
Steven W Flavell 1 , Michael E Greenberg
Affiliation  

Sensory experience and the resulting synaptic activity within the brain are critical for the proper development of neural circuits. Experience-driven synaptic activity causes membrane depolarization and calcium influx into select neurons within a neural circuit, which in turn trigger a wide variety of cellular changes that alter the synaptic connectivity within the neural circuit. One way in which calcium influx leads to the remodeling of synapses made by neurons is through the activation of new gene transcription. Recent studies have identified many of the signaling pathways that link neuronal activity to transcription, revealing both the transcription factors that mediate this process and the neuronal activity-regulated genes. These studies indicate that neuronal activity regulates a complex program of gene expression involved in many aspects of neuronal development, including dendritic branching, synapse maturation, and synapse elimination. Genetic mutations in several key regulators of activity-dependent transcription give rise to neurological disorders in humans, suggesting that future studies of this gene expression program will likely provide insight into the mechanisms by which the disruption of proper synapse development can give rise to a variety of neurological disorders.

中文翻译:

将神经元活动与神经系统的基因表达和可塑性联系起来的信号机制。

大脑内的感官体验和由此产生的突触活动对于神经回路的正常发育至关重要。经验驱动的突触活动导致膜去极化和钙离子流入神经回路内的选定神经元,进而引发多种细胞变化,从而改变神经回路内的突触连接。钙流入导致神经元产生的突触重塑的一种方式是通过激活新基因转录。最近的研究已经确定了许多将神经元活动与转录联系起来的信号通路,揭示了介导这一过程的转录因子和神经元活动调节基因。这些研究表明,神经元活动调节涉及神经元发育许多方面的复杂基因表达程序,包括树突分支、突触成熟和突触消除。活动依赖性转录的几个关键调节因子的基因突变会导致人类神经系统疾病,这表明对该基因表达程序的未来研究可能会提供对正常突触发育破坏可引起各种神经系统疾病的机制的深入了解神经系统疾病。
更新日期:2019-11-01
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