三叉神经节A型神经元核室重组对周围神经末梢炎性损伤的响应。

J Navascues, I Casafont, N T Villagra, M Lafarga, M T Berciano
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引用次数: 8

摘要

在这项研究中,我们利用A型感觉神经节神经元对细胞活动变化的高核反应性来研究参与转录和RNA加工的核室在神经元损伤反应中的重组和动力学。我们采用注射福尔马林对眼/上颌神经分布区周围神经末梢的炎性损伤作为实验模型。我们用免疫荧光和共聚焦激光显微镜对不同核室的特异性抗体进行了分析和超微结构分析。损伤后3天内,神经元损伤的初始反应包括染色质凝聚、乙酰化组蛋白H4表达水平降低、染色质周围颗粒积聚、突出核斑剪接因子重组、Cajal小体数量减少和核仁改变。这些变化倾向于在损伤后第7天恢复,并且与转录和RNA加工的短暂抑制一致。此外,我们还观察到转录因子c-Jun的早期和持续表达。这些结果说明了A型三叉神经元核室的转录依赖性组织,也支持了核反应对轴突损伤的重要性,这是该神经元群体再生能力的关键组成部分。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reorganization of nuclear compartments of type A neurons of trigeminal ganglia in response to inflammatory injury of peripheral nerve endings.

In this study we have taken advantage of the high nuclear responsiveness of type A sensory ganglia neurons to variations of cellular activity to investigate the reorganization and dynamics of nuclear compartments involved in transcription and RNA processing in response to neuronal injury. As experimental model we have used the inflammatory injury of the peripheral nerve endings induced by formalin injection in the areas of ophthalmic/maxillary nerve distribution. We have performed immunofluorescence and confocal laser microscopy analysis with specific antibodies for different nuclear compartments and ultrastructural analysis. The initial response to neuronal injury, within the 3 days post-injury, consisted of chromatin condensation, reduction in the expression level of acetylated histone H4, accumulation of perichromatin granules, reorganization of splicing factors in prominent nuclear speckles, reduction in the number of Cajal bodies and nucleolar alterations. These changes tended to revert by day 7 post-injury and are consistent with a transient inhibition of transcription and RNA processing. Moreover, we have observed an early and sustained expression of the transcription factor c-Jun. These results illustrate the transcription-dependent organization of nuclear compartments in type A trigeminal neurons and also support the importance of the nuclear response to axonal injury as a key component in the regenerative capacity of this neuronal population.

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