谷氨酸神经元在THz波引起的突触可塑性变化中的作用
Lequan Song1, Ji Dong1, Wenjing Cheng1
1Beijing Institute of Radiation Medicine, Beijing 100850, China.
Biomolecules
|April 30, 2025
概括
太赫兹 (THz) 波会损害大脑中的突触可塑性和谷氨酸神经元功能. 激活这些神经元和过度表达GluN2B可以减轻这些不良影响,这表明神经调节是一种治疗方法.
科学领域:
- 神经科学是一个神经科学.
- 生物物理学的生物物理.
- 电力生理学 电力生理学
背景情况:
- 特拉赫兹 (THz) 波,其能量介于毫米波和红外线之间,可能与生物分子相互作用.
- 神经调节和THz波与大脑相互作用的潜在机制仍然不清楚.
研究的目的:
- 为了研究1.94 THz波对小鼠大脑切片中的突触可塑性和谷氨酸性神经元的影响.
- 探索潜在的治疗策略,以减轻THz波引起的神经损伤.
主要方法:
- 暴露小鼠大脑切片到1.94 THz波.
- 使用传输电子显微镜 (TEM),长期潜能 (LTP) 和分子标记物 (Tuj1,SYN) 评估突触可塑性.
- 评估谷氨酸性神经元活动,N-甲基-D-酸盐受体 (NMDAR) 功能,以及通过光遗传学,化学遗传学和GluN2B. lentiviral过度表达的调制.
主要成果:
- THz波暴露降低了突触可塑性,谷氨酸性神经元活动和NMDAR功能.
- 激发神经元的光遗传/化学遗传激活和GluN2B过度表达改善了THz诱导的突触损伤.
- THz波降低了 postsynaptic密度厚度,fEPSP斜率和突触标记物的表达.
结论:
- 1.94 THz波对突触可塑性和谷氨酸质传输在腹部海马体CA1 (vCA1) 中产生负面影响.
- 神经调节,特别是通过谷氨酸性神经元激活或GluN2B增强,提供了一种潜在的治疗方法来对抗THz辐射的不良影响.
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