The endocannabinoid system is involved in the anxiety-like behavior induced by dual-frequency 2.65/0.8 GHz electromagnetic radiation in mice

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2024-04-15 DOI:10.3389/fnmol.2024.1366855

Teng Xue, Rui-Han Ma, Chou Xu, Bin Sun, Dong-Fei Yan, Xiao-Man Liu, Dawen Gao, Zhi-Hui Li, Yan Gao, Chang-Zhen Wang

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引用次数: 0

Abstract

As wireless communication devices gain popularity, concerns about the potential risks of environmental exposure to complex frequency electromagnetic radiation (EMR) on mental health have become a public health issue. Historically, EMR research has predominantly focused on single- frequency electromagnetic waves, neglecting the study of multi-frequency electromagnetic waves, which more accurately represent everyday life. To address these concerns, our study compared the emotional effects of single-frequency and dual-frequency EMR while exploring potential molecular mechanisms and intervention targets. Our results revealed that single-frequency EMR at 2.65 or 0.8 GHz did not induce anxiety-like behavior in mice. However, exposure to dual-frequency EMR at 2.65/0.8 GHz significantly led to anxiety-like behavior in mice. Further analysis of mouse sera revealed substantial increases in corticosterone and corticotrophin releasing hormone levels following exposure to 2.65/0.8 GHz EMR. Transcriptome sequencing indicated a significant decrease in the expression of Cnr1, encoding cannabinoid receptor 1 Type (CB1R), in the cerebral. This finding was consistently verified through western blot analysis, revealing a substantial reduction in CB1R content. Additionally, a significant decrease in the endocannabinoid 2-arachidonoylglycerol was observed in the cerebral cortex. Remarkably, administering the cannabinoid receptor agonist Win55-212-2 significantly alleviated the anxiety-like behavior, and the cannabinoid receptor antagonist AM251 effectively counteracted the anti-anxiety effects of Win55-212-2. In summary, our research confirmed that dual-frequency EMR is more likely to induce anxiety-like behavior in mice than single-frequency EMR, with implications for the hypothalamic–pituitary–adrenal axis and the endocannabinoid system. Furthermore, our findings suggest that Win55-212-2 may represent a novel avenue for researching and developing anti-EMR drugs.

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内源性大麻素系统参与了双频 2.65/0.8 GHz 电磁辐射诱导小鼠焦虑样行为的过程

随着无线通信设备的普及，人们开始关注暴露于环境中的复合频率电磁辐射（EMR）对心理健康的潜在风险，这已成为一个公共卫生问题。一直以来，电磁辐射研究主要集中于单频电磁波，而忽视了对更能准确反映日常生活的多频电磁波的研究。为了解决这些问题，我们的研究比较了单频和双频电磁波对情绪的影响，同时探讨了潜在的分子机制和干预目标。我们的研究结果表明，2.65 或 0.8 千兆赫的单频电磁辐射不会诱发小鼠的焦虑行为。然而，暴露于 2.65/0.8 GHz 的双频电磁辐射会显著导致小鼠的焦虑样行为。对小鼠血清的进一步分析表明，暴露于 2.65/0.8 GHz 电磁辐射后，皮质酮和促肾上腺皮质激素释放激素的水平大幅上升。转录组测序表明，大脑中编码大麻素受体 1 型（CB1R）的 Cnr1 的表达量显著下降。这一发现在 Western 印迹分析中得到了一致验证，显示 CB1R 含量大幅减少。此外，还观察到大脑皮层中的内源性大麻素-2-丙烯酰甘油明显减少。值得注意的是，给予大麻素受体激动剂 Win55-212-2 能明显缓解焦虑样行为，而大麻素受体拮抗剂 AM251 能有效抵消 Win55-212-2 的抗焦虑作用。总之，我们的研究证实，双频电磁辐射比单频电磁辐射更容易诱发小鼠的焦虑样行为，这对下丘脑-垂体-肾上腺轴和内源性大麻素系统都有影响。此外，我们的研究结果表明，Win55-212-2 可能是研究和开发抗电磁辐射药物的一个新途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.