Hao Yanhui, Li Wenchao, Wang Hui, Zhang Jing, Yu Chao, Tan Shengzhi, Wang Haoyu, Xu Xinping, Dong Ji, Yao Binwei, Zhou Hongmei, Zhao Li, Peng Ruiyun
Department of Experimental Pathology, Institute of Radiation Medicine, Beijing, PR China.
Division of Radiation Protection and Health Physics, Institute of Radiation Medicine, Beijing, PR China.
Physiol Behav. 2018 May 1;188:119-127. doi: 10.1016/j.physbeh.2018.02.005. Epub 2018 Feb 3.
To explore how autophagy changes and whether autophagy is involved in the pathophysiological process of synaptic plasticity injury caused by microwave radiation, we established a 30 mW/cm microwave-exposure in vivo model, which caused reversible injuries in rat neurons. Microwave radiation induced cognitive impairment in rats and synaptic plasticity injury in rat hippocampal neurons. Autophagy in rat hippocampal neurons was activated following microwave exposure. Additionally, we observed that synaptic vesicles were encapsulated by autophagosomes, a phenomenon more evident in the microwave-exposed group. Colocation of autophagosomes and synaptic vesicles in rat hippocampal neurons increased following microwave exposure.
microwave exposure led to the activation of autophagy in rat hippocampal neurons, and excessive activation of autophagy might damage synaptic plasticity by mediating synaptic vesicle degradation.
为探究自噬如何变化以及自噬是否参与微波辐射引起的突触可塑性损伤的病理生理过程，我们建立了30 mW/cm微波体内暴露模型，该模型可导致大鼠神经元可逆性损伤。微波辐射诱导大鼠认知功能障碍和大鼠海马神经元突触可塑性损伤。微波暴露后大鼠海马神经元自噬被激活。此外，我们观察到突触小泡被自噬体包裹，这种现象在微波暴露组中更明显。微波暴露后大鼠海马神经元中自噬体与突触小泡的共定位增加。
微波暴露导致大鼠海马神经元自噬激活，自噬的过度激活可能通过介导突触小泡降解而损害突触可塑性。
