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应激通过糖皮质激素受体依赖性转录程序增加周围轴突的生长和再生。

Stress Increases Peripheral Axon Growth and Regeneration through Glucocorticoid Receptor-Dependent Transcriptional Programs.

机构信息

Center for Brain and Spinal Cord Repair, Department of Neuroscience, Wexner Medical Center at the Ohio State University, Columbus, OH 43210.

The Miami Project to Cure Paralysis, Department of Neurological Surgery, The University of Miami, Miami, FL 33136.

出版信息

eNeuro. 2017 Aug 21;4(4). doi: 10.1523/ENEURO.0246-17.2017. eCollection 2017 Jul-Aug.

Abstract

Stress and glucocorticoid (GC) release are common behavioral and hormonal responses to injury or disease. In the brain, stress/GCs can alter neuron structure and function leading to cognitive impairment. Stress and GCs also exacerbate pain, but whether a corresponding change occurs in structural plasticity of sensory neurons is unknown. Here, we show that in female mice () basal GC receptor (, also known as GR) expression in dorsal root ganglion (DRG) sensory neurons is 15-fold higher than in neurons in canonical stress-responsive brain regions (). In response to stress or GCs, adult DRG neurite growth increases through mechanisms involving GR-dependent gene transcription. , prior exposure to an acute systemic stress increases peripheral nerve regeneration. These data have broad clinical implications and highlight the importance of stress and GCs as novel behavioral and circulating modifiers of neuronal plasticity.

摘要

压力和糖皮质激素(GC)的释放是对损伤或疾病的常见行为和激素反应。在大脑中,压力/GC 可以改变神经元的结构和功能,导致认知障碍。压力和 GCs 也会加剧疼痛,但感觉神经元的结构可塑性是否会发生相应变化尚不清楚。在这里,我们发现,在雌性小鼠中,背根神经节(DRG)感觉神经元中的基础 GC 受体(也称为 GR)表达水平比在经典应激反应脑区中的神经元高 15 倍()。在应激或 GCs 的作用下,成年 DRG 神经元轴突生长增加,其机制涉及 GR 依赖性基因转录。此外,先前暴露于急性全身应激会增加周围神经再生。这些数据具有广泛的临床意义,强调了压力和 GCs 作为神经元可塑性的新型行为和循环调节剂的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c48/5563843/c775a453a6f1/enu0041723840001.jpg

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