Role of BDNF signaling for striatal plasticity and motor learning (A05)

BDNF 信号对纹状体可塑性和运动学习的作用 (A05)

• 批准号: 446026919
• 金额: --
• 依托单位: Institut für Klinische Neurobiologie
• 依托单位国家: 德国
• 项目类别: CRC/Transregios
• 财政年份: 2020
• 资助国家: 德国
• 起止时间: 2019-12-31 至 2023-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/446026919?language=en
• 关键词: Role; BDNF; signaling; striatal; plasticity

This project is designed to investigate how the release of brain-derived neurotrophic factor (BDNF) from corticostriatal afferents and tropomyosin receptor kinase B (TrkB) responsiveness in striatal medium spiny neurons are regulated by dopaminergic activity from the substantia nigra and by deep brain stimulation (DBS) of the subthalamic nucleus (STN). The project builds on our expertise with cell culture techniques for enrichment of medium spiny neurons and new mouse models of dystonia, as well as models in which BDNF signaling in these corticostriatal synapses is disturbed. The goal is to understand how plasticity mechanisms at this synapse contribute to motor defects in Parkinson´s disease and dystonia, and how DBS of the STN modulates this synapse and motor function.

本研究旨在探讨黑质多巴胺能神经元和丘脑底核脑深部电刺激（DBS）对皮质纹状体传入神经释放脑源性神经营养因子（BDNF）和纹状体中型棘状神经元原肌球蛋白受体激酶B（Trk B）反应性的调节作用。该项目建立在我们的专业知识与细胞培养技术的富集中棘神经元和新的小鼠模型的肌张力障碍，以及模型中，BDNF信号在这些皮质纹状体突触被扰乱。目的是了解该突触的可塑性机制如何导致帕金森病和肌张力障碍的运动缺陷，以及脑深部电刺激如何调节该突触和运动功能。