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微波暴露通过过度激活NMDA受体信号通路损害大鼠海马体和PC12细胞中的突触可塑性。

Microwave exposure impairs synaptic plasticity in the rat hippocampus and PC12 cells through over-activation of the NMDA receptor signaling pathway.

作者信息

Xiong Lu, Sun Cheng Feng, Zhang Jing, Gao Ya Bing, Wang Li Feng, Zuo Hong Yan, Wang Shui Ming, Zhou Hong Mei, Xu Xin Ping, Dong Ji, Yao Bin Wei, Zhao Li, Peng Rui Yun

机构信息

Beijing Institute of Radiation Medicine, Beijing 100850, China.

出版信息

Biomed Environ Sci. 2015 Jan;28(1):13-24. doi: 10.3967/bes2015.002.

Abstract

OBJECTIVE

The aim of this study is to investigate whether microwave exposure would affect the N-methyl-D-aspartate receptor (NMDAR) signaling pathway to establish whether this plays a role in synaptic plasticity impairment.

METHODS

48 male Wistar rats were exposed to 30 mW/cm2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H&E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated.

RESULTS

Microwave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits (NR1, NR2A, and NR2B) and related signaling molecules (Ca2+/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein) were examined.

CONCLUSION

30 mW/cm2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity.

摘要

目的

本研究旨在探究微波暴露是否会影响N-甲基-D-天冬氨酸受体(NMDAR)信号通路,以确定其是否在突触可塑性损伤中起作用。

方法

48只雄性Wistar大鼠每隔一天暴露于30 mW/cm2微波下10分钟,共三次。通过苏木精-伊红染色和透射电子显微镜观察海马结构。将PC12细胞暴露于30 mW/cm2微波下5分钟,并用扫描电子显微镜和原子力显微镜观察突触形态。检测氨基酸神经递质的释放和钙内流。评估几种关键NMDAR信号分子的表达。

结果

微波暴露导致大鼠海马结构和PC12细胞损伤,尤其是突触的结构和数量。PC12细胞中谷氨酸和γ-氨基丁酸神经递质的比例增加,细胞内钙水平升高。检测到NMDAR亚基(NR1、NR2A和NR2B)及相关信号分子(钙/钙调蛋白依赖性蛋白激酶IIγ和磷酸化环磷酸腺苷反应元件结合蛋白)有显著变化。

结论

30 mW/cm2微波暴露导致突触结构、氨基酸神经递质释放和钙内流改变。NMDAR信号分子与突触可塑性受损密切相关。

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