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在实验性脑疟疾中,与FGF14相聚的TNFR1信号控制神经元过活和疾病行为

Nolan M Dvorak¹, Nadia D Domingo^2,3, Cynthia M Tapia¹

¹Department of Pharmacology & Toxicology, University of Texas Medical Branch, Galveston, TX, 77555, USA.

Journal of neuroinflammation

|December 20, 2023

概括

过多的瘤亡因子 (TNF) 驱动实验性脑疟疾 (eCM) 神经炎症. 这项研究揭示了纤维细胞生长因子14 (FGF14) 作为神经元过敏和eCM疾病行为的关键调解者,建议它作为治疗点.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
病理学病理学病理学

背景情况:

过度的瘤亡因子 (TNF) 有助于高炎症的实验性脑疟疾 (eCM) 病原体.
在eCM期间TNF在神经元功能障碍中的确切作用尚不清楚.
这项研究调查了TNF驱动的神经元刺激性变化和eCM中的信号通路.

研究的目的:

阐明eCM对神经元刺激性的电生理后果.
识别eCM中TNF诱导的神经元功能障碍背后的细胞信号机制.
调查针对eCM中已识别的途径的治疗潜力.

主要方法:

分裂-露西法酶补充试验 (LCA) 研究瘤坏死因子受体1 (TNFR1) 的下游信号.
来自eCM小鼠的大脑切片中的全细胞补丁电生理学,以评估CA1金字塔神经元刺激性.
在体内基因沉默以评估信号分子在eCM诱导的行为变化中的作用.

主要成果:

通过TNFR1刺激TNF,通过Janus Kinase 2 (JAK2) 增加纤维细胞生长因子14 (FGF14) 和电压导入通道1.6 (Na_v1.6) 的复杂组合.
青杆菌感染通过TNFR1-JAK2-FGF14-Nav1.6通路在CA1金字塔神经元中增加Na_v1.6通道导电,导致过度兴奋.
抗TNF抗体和FGF14基因沉默在CA1中减轻了神经元过敏性和减少了eCM中的疾病行为.

结论:

在TNFR1-JAK2-FGF14-Na_v1.6信号网络中介TNF诱导的神经元过刺激性在eCM.
FGF14是eCM中神经炎症级联的关键组成部分.
抑制FGF14为管理eCM中神经炎症和相关症状提供了潜在的治疗策略.

关键词:

在海马体内,海马体离子通道的离子通道神经炎症是一种神经炎症.神经元刺激性的神经元刺激性酸化是指酸化的方法.突触性可塑性突触性可塑性治疗目标治疗目标

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