创伤性脑损伤引起的嗅球炎症变化破坏神经网络,导致嗅觉功能障碍
Xiang Liu1, Zhuofan Lei1, Dylan Gilhooly2
1Department of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Brain, behavior, and immunity
|August 9, 2023
概括
创伤性脑损伤 (TBI) 通过触发嗅球 (OB) 中的炎症和神经元功能障碍引起嗅觉缺陷. 准Hv1/NOX2通路可能会在TBI后恢复嗅觉功能.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 眼科医生 眼科 眼科
背景情况:
- 创伤性脑损伤 (TBI) 经常导致嗅觉缺陷 (OD),影响生活质量和认知功能.
- 与TBI相关的OD背后的机制仍然不太清楚,对实验模型的研究有限.
研究的目的:
- 在实验性TBI后,研究嗅球 (OB) 中的炎症和神经元功能障碍.
- 阐明电压关闭的质子通道Hv1和NOX2在TBI引起的OD中的作用.
主要方法:
- 在雄性小鼠中使用受控皮质冲击 (CCI) 模型来诱导TBI.
- 评估了OB炎症,神经元活动和嗅觉行为.
- 研究了Hv1和NOX2淘汰赛 (KO) 和NOX2抑制剂 (NOX2ds-tat) 的作用.
主要成果:
- 创伤诱导了快速和持续的OB炎症,其特征是炎症性细胞因子升高和免疫细胞透.
- 微质/巨细胞中HV1和NOX2的升高与增加的活性氧物种生产相关.
- 缺少Hv1改善了神经元活动,Hv1 KO和NOX2 KO小鼠的OD都减少了.
- 通过鼻内输送抑制NOX2,改善了创伤后的OD.
结论:
- 由HV1/NOX2通路介导的OB炎症和神经元功能障碍,在TBI相关的嗅觉缺陷中至关重要.
- Hv1和NOX2代表了TBI后减轻嗅觉功能障碍的潜在治疗点.
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