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长期暴露于2.45 GHz微波辐射可改善血管性痴呆模型中的认知和突触可塑性损伤。

Chronic exposure to 2.45 GHz microwave radiation improves cognition and synaptic plasticity impairment in vascular dementia model.

作者信息

Bayat Mahnaz, Karimi Narges, Karami Mohammad, Haghighi Afshin Borhani, Bayat Kamjoo, Akbari Somayeh, Haghani Masoud

机构信息

Clinical Neurology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran.

Department of Physiology, the Medical School, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Int J Neurosci. 2023 Feb;133(2):111-122. doi: 10.1080/00207454.2021.1896502. Epub 2021 Mar 11.

DOI:10.1080/00207454.2021.1896502
PMID:33635159
Abstract

In this study, we evaluated the effects of 2.45 GHz microwave radiation on cognitive dysfunction induced by vascular dementia (VaD). The VaD was induced by bilateral-common carotid occlusion (2-VO). The rats were divided into 4 groups including: control ( = 6), sham ( = 6), 2-VO ( = 8), and 2-VO + Wi-Fi ( = 10) groups. Wi-Fi modem centrally located at the distance of 25 cm from the animal's cages and the animals were continuously exposed to Wi-Fi signal while they freely moved in the cage (2 h/day for forty-five days). Therefore, the power density (PD) and specific absorption rate value (SAR) decreased at a distance of 25 to 60 cm (PD = 0.018 to 0.0032 mW/cm, SAR = 0.0346 to 0.0060 W/Kg). The learning, memory, and hippocampal synaptic-plasticity were evaluated by radial arm maze (RAM), passive avoidance (PA), and field-potential recording respectively. The number of hippocampal CA1 cells was also assessed by giemsa staining. Our results showed that VaD model led to impairment in the spatial learning and memory performance in RAM and PA that were associated with long-term potentiation (LTP) impairment, decrease of basal-synaptic transmission (BST), increase of GABA transmission, and decline of neurotransmitter release-probability as well as hippocampal cell loss. Notably, chronic Wi-Fi exposure significantly recovered the learning-memory performance, LTP induction, and cell loss without any effect on BST. The LTP recovery by Wi-Fi in the 2-VO rats was probably related to significant increases in the hippocampal CA1 neuronal density, partial recovery of neurotransmitter release probability, and reduction of GABA transmissiSon as evident by rescue of paired-pulse ratio 10 ms.

摘要

在本研究中,我们评估了2.45 GHz微波辐射对血管性痴呆(VaD)所致认知功能障碍的影响。VaD由双侧颈总动脉闭塞(2-VO)诱导产生。大鼠被分为4组,包括:对照组(n = 6)、假手术组(n = 6)、2-VO组(n = 8)和2-VO + Wi-Fi组(n = 10)。Wi-Fi调制解调器位于距离动物笼25 cm处,动物在笼中自由活动时持续暴露于Wi-Fi信号下(每天2小时,共45天)。因此,在25至60 cm的距离处,功率密度(PD)和比吸收率值(SAR)降低(PD = 0.018至0.0032 mW/cm²,SAR = 0.0346至0.0060 W/Kg)。分别通过放射状臂迷宫(RAM)、被动回避(PA)和场电位记录来评估学习、记忆和海马突触可塑性。还通过吉姆萨染色评估海马CA1区细胞数量。我们的结果表明,VaD模型导致RAM和PA中的空间学习和记忆表现受损,这与长时程增强(LTP)受损、基础突触传递(BST)减少、GABA传递增加、神经递质释放概率下降以及海马细胞丢失有关。值得注意的是,慢性Wi-Fi暴露显著恢复了学习记忆表现、LTP诱导和细胞丢失,而对BST没有任何影响。Wi-Fi使2-VO大鼠的LTP恢复可能与海马CA1神经元密度显著增加、神经递质释放概率部分恢复以及GABA传递减少有关,10 ms配对脉冲比率的恢复证明了这一点。

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