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短波辐照后大鼠海马行为异常及 NMDA 受体相关 CREB 抑制

Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus after Shortwave Exposure.

机构信息

Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China.

出版信息

Biomed Environ Sci. 2019 Mar;32(3):189-198. doi: 10.3967/bes2019.026.

DOI:10.3967/bes2019.026
PMID:30987693
Abstract

OBJECTIVE

To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms.

METHODS

One hundred Wistar rats were randomly divided into four groups (25 rats per group) and exposed to 27 MHz continuous shortwave at a power density of 5, 10, or 30 mW/cm2 for 6 min once only or underwent sham exposure for the control. The spatial learning and memory, electroencephalogram (EEG), hippocampal structure and Nissl bodies were analysed. Furthermore, the expressions of N-methyl-D-aspartate receptor (NMDAR) subunits (NR1, NR2A, and NR2B), cAMP responsive element-binding protein (CREB) and phosphorylated CREB (p-CREB) in hippocampal tissue were analysed on 1, 7, and 14 days after exposure.

RESULTS

The rats in the 10 and 30 mW/cm2 groups had poor learning and memory, disrupted EEG oscillations, and injured hippocampal structures, including hippocampal neurons degeneration, mitochondria cavitation and blood capillaries swelling. The Nissl body content was also reduced in the exposure groups. Moreover, the hippocampal tissue in the 30 mW/cm2 group had increased expressions of NR2A and NR2B and decreased levels of CREB and p-CREB.

CONCLUSION

Shortwave exposure (27 MHz, with an average power density of 10 and 30 mW/cm2) impaired rats' spatial learning and memory and caused a series of dose-dependent pathophysiological changes. Moreover, NMDAR-related CREB pathway suppression might be involved in shortwave-induced structural and functional impairments in the rat hippocampus.

摘要

目的

评估短波辐射对大鼠海马结构和功能的有害影响,并探讨其潜在机制。

方法

将 100 只 Wistar 大鼠随机分为四组(每组 25 只),分别接受 27 MHz 连续短波辐射,功率密度分别为 5、10 或 30 mW/cm2,单次照射 6 分钟,或进行假照射作为对照。分析空间学习和记忆、脑电图(EEG)、海马结构和尼氏小体。此外,还分析了海马组织中 N-甲基-D-天冬氨酸受体(NMDAR)亚基(NR1、NR2A 和 NR2B)、环磷酸腺苷反应元件结合蛋白(CREB)及其磷酸化形式(p-CREB)在照射后 1、7 和 14 天的表达情况。

结果

10 和 30 mW/cm2 组大鼠学习记忆能力差,脑电图振荡紊乱,海马结构损伤,包括海马神经元变性、线粒体空泡化和毛细血管肿胀。暴露组的尼氏小体含量也减少。此外,30 mW/cm2 组大鼠海马组织中 NR2A 和 NR2B 的表达增加,CREB 和 p-CREB 的水平降低。

结论

短波辐射(27 MHz,平均功率密度为 10 和 30 mW/cm2)损害大鼠的空间学习和记忆能力,并引起一系列与剂量相关的病理生理变化。此外,NMDAR 相关的 CREB 通路抑制可能参与了短波诱导的大鼠海马结构和功能损伤。

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