通过miRNA介导的基菲林合成控制驱动持续的抑制性突触可塑性
Theresa M Welle1,2, Dipen Rajgor1,2, Joshua D Garcia1
1Department of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045.
bioRxiv : the preprint server for biology
|January 3, 2024
概括
微RNA 153 (miR153) 控制着基菲林翻译,这是抑制突触的关键蛋白质. 抑制性长期强化 (iLTP) 降低 miR153 的调节,促进基菲林合成以加强突触.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 突触性可塑性 突触性可塑性
背景情况:
- 活动依赖的蛋白质合成对于长期的突触可塑性至关重要.
- 在抑制性突触中调节翻译的机制尚不清楚.
- 抑制性长期强化 (iLTP) 通过增加GABAAR和gephyrin集群来加强抑制性突触.
结论:
- 描述了一种新的微RNA依赖的转录后机制,可以控制gephyrin的表达.
- 这一途径对于维持抑制性突触可塑性至关重要.
- 表明miRNA路径的融合,以协调突触可塑性的基因表达.
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