微质细胞通过互惠的fractalkine和adenosine信号调节运动神经元的可塑性
Alexandria B Marciante1, Arash Tadjalli1,2, Maria Nikodemova1
1Breathing Research and Therapeutics Center, Department of Physical Therapy and McKnight Brain Institute, University of Florida, Gainesville, FL, USA.
Nature communications
|November 28, 2024
概括
微质细胞调节运动神经元中的呼吸可塑性. 急性间歇性缺氧 (AIH) 触发了涉及fractalkines和腺的信号通路,根据缺氧严重程度影响了性长期促进 (pLTF).
科学领域:
- 神经科学是一个神经科学.
- 呼吸系统生理学 呼吸系统生理学
- 细胞生物学 细胞生物学
背景情况:
- 脑膜长期促进 (pLTF) 是一种呼吸机运动可塑性的形式.
- pLTF是由血清和腺信号调节的.
- 目前,PLTF中腺的来源尚不清楚.
研究的目的:
- 调查微质在神经运动神经元的神经可塑性中的作用.
- 确定急性间歇性缺氧 (AIH) 是否启动了动神经元和微质之间分素信号传递.
- 阐明细胞外腺素形成的机制及其对pLTF的影响.
主要方法:
- 在雄性大鼠中使用神经生理学制剂.
- 操纵的碎素信号传输 (敲击和受体抑制).
- 在不同的AIH严重程度下使用微质切除和评估pLTF.
主要成果:
- 适度的AIH:由动神经元激活腺素2A受体可以抑制血清主导的pLTF.
- 严重的AIH:依赖于腺的机制诱导了pLTF.
- 调节微质骨素信号,以依赖于AIH严重程度的方式改变了pLTF.
结论:
- 微质细胞在神经神经元中调节神经可塑性方面发挥着重要作用.
- 微质骨蛋白信号传递有助于腺的产生,影响呼吸机运动可塑性.
- 微质活动的平衡对于调整呼吸反应以适应缺氧至关重要.
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