Wang Hui, Tan Shengzhi, Zhao Li, Dong Ji, Yao Binwei, Xu Xinping, Zhang Bo, Zhang Jing, Zhou Hongmei, Peng Ruiyun
Cell Physiol Biochem. 2018;51(1):97-112. doi: 10.1159/000495167. Epub 2018 Nov 15.
BACKGROUND/AIMS: The N-methyl-D-aspartic acid receptor (NMDAR) has been extensively studied for its important roles in synaptic plasticity and learning and memory. However, the effects of microwave radiation on the subunit composition and activity of NMDARs and the relationship between NMDARs and microwave-induced synaptic plasticity have not been thoroughly elucidated to date.
In our study, primary hippocampal neurons were used to evaluate the effects of microwave radiation on synaptic plasticity. Structural changes were observed by diolistic (Dil) labeling and scanning electron microscopy (SEM) observation. Functional synaptic plasticity was reflected by the NMDAR currents, which were detected by whole cell patch clamp. We also detected the expression of NMDAR subunits by real-time PCR and Western blot analysis. To clarify the effects of microwave radiation on NMDAR-induced synaptic plasticity, suitable agonists or inhibitors were added to confirm the role of NMDARs on microwave-induced synaptic plasticity. Dil labeling, SEM observation, whole cell patch clamp, real-time PCR and Western blot analysis were used to evaluate changes in synaptic plasticity after treatment with agonists or inhibitors.
Our results found that microwave exposure impaired neurite development and decreased mRNA and protein levels and the current density of NMDARs. Due to the decreased expression of NMDAR subunits after microwave exposure, the selective agonist NMDA was added to identify the role of NMDARs on microwave-induced synaptic plasticity injuries. After adding the agonist, the expression of NMDAR subunits recovered to the normal levels. In addition, the microwave-induced structural and functional synaptic plasticity injuries recovered, including the number and length of neurites, the connections between neurons, and the NMDAR current.
Microwave radiation caused neuronal synaptic plasticity injuries in primary hippocampal neurons, and NMDARs played protective roles on the damage process.
背景/目的：N-甲基-D-天冬氨酸受体（NMDAR）因其在突触可塑性以及学习和记忆中的重要作用而受到广泛研究。然而，微波辐射对NMDAR亚基组成和活性的影响以及NMDAR与微波诱导的突触可塑性之间的关系迄今尚未得到充分阐明。
在我们的研究中，原代海马神经元被用于评估微波辐射对突触可塑性的影响。通过荧光金（Dil）标记和扫描电子显微镜（SEM）观察来观察结构变化。功能性突触可塑性通过NMDAR电流来反映，该电流通过全细胞膜片钳检测。我们还通过实时PCR和蛋白质印迹分析检测了NMDAR亚基的表达。为了阐明微波辐射对NMDAR诱导的突触可塑性的影响，添加了合适的激动剂或抑制剂以确认NMDAR在微波诱导的突触可塑性中的作用。荧光金标记、SEM观察、全细胞膜片钳、实时PCR和蛋白质印迹分析被用于评估用激动剂或抑制剂处理后突触可塑性的变化。
我们的结果发现，微波暴露损害了神经突发育，降低了NMDAR的mRNA和蛋白质水平以及电流密度。由于微波暴露后NMDAR亚基的表达降低，添加了选择性激动剂N-甲基-D-天冬氨酸（NMDA）以确定NMDAR在微波诱导的突触可塑性损伤中的作用。添加激动剂后，NMDAR亚基的表达恢复到正常水平。此外，微波诱导的结构和功能性突触可塑性损伤得到恢复，包括神经突的数量和长度、神经元之间的连接以及NMDAR电流。
微波辐射在原代海马神经元中引起神经元突触可塑性损伤，并且NMDAR在损伤过程中发挥保护作用。
