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A certain power of microwave radiation could cause changes in the nervous, cardiovascular, and other systems of the body, and the brain was a sensitive target organ of microwave radiation injury. Studies have shown that microwaves can impair cognitive functions in humans and animals, such as learning and memory, attention, and orientation. The dose-dependent effect of microwave radiation is still unclear. Our study aimed to investigate the effects of 1.5-GHz microwaves with different average power densities on locative learning and memory abilities, hippocampal structure, and related N-methyl D-aspartate receptor (NMDAR) signalling pathway proteins in rats. A total number of 140 male Wistar rats were randomly divided into four groups: S group (sham exposure), L5 group (1.5-GHz microwaves with average power density = 5 mW/cm 2 ), L30 group (1.5-GHz microwaves with average power density = 30 mW/cm 2 ), and L50 group (1.5-GHz microwaves with average power density = 50 mW/cm 2 ). Changes in spatial learning and memory, EEG activity, hippocampal structure, and NMDAR signalling pathway molecules were detected from 6 h to 28 d after microwave exposure. After exposure to 1.5-GHz microwaves, rats in the L30 and L50 groups showed impaired spatial memory, inhibited EEG activity, pyknosis and hyperchromatism of neuron nucleus, and changes in NMDAR subunits and downstream signalling molecules. In conclusion, 1.5-GHz microwaves with an average power density of 5, 30, and 50 mW/cm 2 could induce spatial memory dysfunction, hippocampal structure changes, and changes in protein levels in rats, and there was a defined dose-dependent effect., (© 2022. The Author(s).)

This study aimed to evaluate the acute effects of 2.856 GHz and 1.5 GHz microwaves on spatial memory and cAMP response element binding (CREB)-related pathways. A total of 120 male Wistar rats were divided into four groups: a control group (C); 2.856 GHz microwave exposure group (S group); 1.5 GHz microwave exposure group (L group); and 2.856 and 1.5 GHz cumulative exposure group (SL group). Decreases in spatial memory abilities, changes in EEG, structural injuries, and the downregulation of phosphorylated-Ak strain transforming (p-AKT), phosphorylated-calcium/calmodulin-dependent protein kinase II (p-CaMKII), phosphorylated extracellular signal regulated kinase (p-ERK) and p-CREB was observed 6 h after microwave exposure. Significant differences in the expression of p-CaMKII were found between the S and L groups. The power amplitudes of the EEG waves (θ, δ), levels of structural injuries and the expression of p-AKT, p-CaMK II, p-CREB, and p-ERK1/2 were significantly different in the S and L groups compared to the SL group. Interaction effects between the 2.856 and 1.5 GHz microwaves were found in the EEG and p-CREB changes. Our findings indicated that 2.856 GHz and 1.5 GHz microwave exposure induced a decline in spatial memory, which might be related to p-AKT, p-CaMK II, p-CREB and p-ERK1/2.

Background: Abnormal release of neurotransmitters after microwave exposure can cause learning and memory deficits. This study investigated the mechanism of this effect by exploring the potential role of phosphorylated synapsin I (p-Syn I)., Methods: Wistar rats, rat hippocampal synaptosomes, and differentiated (neuronal) PC12 cells were exposed to microwave radiation for 5 min at a mean power density of 30 mW/cm2. Sham group rats, synaptosomes, and cells were otherwise identically treated and acted as controls for all of the following post-exposure analyses. Spatial learning and memory in rats was assessed using the Morris Water Maze (MWM) navigation task. The protein expression and presynaptic distribution of p-Syn I and neurotransmitter transporters were examined via western blotting and immunoelectron microscopy, respectively. Levels amino acid neurotransmitter release from rat hippocampal synaptosomes and PC12 cells were measured using high performance liquid chromatograph (HPLC) at 6 hours after exposure, with or without synapsin I silencing via shRNA transfection., Results: In the rat experiments, there was a decrease in spatial memory performance after microwave exposure. The expression of p-Syn I (ser-553) was decreased at 3 days post-exposure and elevated at later time points. Vesicular GABA transporter (VGAT) was significantly elevated after exposure. The GABA release from synaptosomes was attenuated and p-Syn I (ser-553) and VGAT were both enriched in small clear synaptic vesicles, which abnormally assembled in the presynaptic terminal after exposure. In the PC12 cell experiments, the expression of p-Syn I (ser-553) and GABA release were both attenuated at 6 hours after exposure. Both microwave exposure and p-Syn I silencing reduced GABA release and maximal reduction was found for the combination of the two, indicating a synergetic effect., Conclusion: p-Syn I (ser-553) was found to play a key role in the impaired GABA release and cognitive dysfunction that was induced by microwave exposure.

Previous studies have suggested that microwave (MW) radiation with certain parameters can induce spatial memory deficits. However, the effect of MW on the topological organization of the brain network is still unknown. This work aimed to investigate the topological organization of the brain network in rats with spatial memory impairments induced by acute microwave (MW) radiation. The Morris water maze (MWM) test and resting-state functional magnetic resonance imaging were performed to estimate the spatial memory ability and brain network topological organization of the rats after MW exposure. Compared with the sham group, the rats exposed to 30 mW/cm2 1.5 GHz MW radiation exhibited a significantly decreased normalized clustering coefficient (γ) (p = 0.002) 1 d after the exposure and a prolonged average escape latency (AEL) (p = 0.014) 3 d after the exposure. Moreover, after 10 mW/cm2 1.5 GHz MW radiation, a significantly decreased γ (p = 0.003) was also observed in the rats, without any changes in AEL. In contrast, no adverse effects on AEL or topological parameters were observed after 9.375 GHz MW radiation. In conclusion, the rats with spatial memory deficits induced by MW radiation exhibited disruptions in the topological organization of the brain network. Moreover, these topological organization disruptions emerged earlier than behavioral symptom onset and could even be found in the rats without a decline in the performance of the spatial memory task. Therefore, it is possible to use the topological parameters of the brain network as early and sensitive indicators of the spatial memory impairments induced by acute MW radiation. [ABSTRACT FROM AUTHOR]

This study aimed to elucidate the effects and biological targets sensitive to simultaneous 1.5 and 4.3 GHz microwave exposure in rats. A total of 120 male Wistar rats were divided randomly into four groups: the sham (S group), 1.5 GHz microwave exposure (L group), 4.3 GHz microwave exposure (C group) and simultaneous 1.5 and 4.3 GHz microwave exposure (LC group) groups. Spatial learning and memory, cortical electrical activity, and hippocampal ultrastructure were assessed by the Morris Water Maze, electroencephalography, and transmission electron microscopy, respectively. Additionally, serum exosomes were isolated by ultracentrifugation and assessed by Western blotting, nanoparticle tracking and transmission electron microscopy. The serum exosome protein content was assessed by label-free quantitative proteomics. Impaired spatial learning and memory decreased cortical excitability, and damage to the hippocampal ultrastructure were observed in groups exposed to microwaves, especially the L and LC groups. A total of 54, 145 and 296 exosomal proteins were differentially expressed between the S group and the L, C and LC groups, respectively. These differentially expressed proteins were involved in the synaptic vesicle cycle and SNARE interactions during vesicular transport. Additionally, VAMP8, Syn7 and VMAT are potential serum markers of simultaneous microwave exposure. Thus, exposure to 1.5 and 4.3 GHz microwaves induced impairments in spatial learning and memory, and simultaneous microwave exposure had the most severe effects. • A microwave source with simultaneous exposure of 1.5 GHz and 4.3 GHz was constructed. • The simultaneous microwave could induced early impairments spatial learning and memory abilities and hippocampal structure. • VAMP8, Syn7, VMAT might be key molecules in serum exosomes for microwave exposure. [ABSTRACT FROM AUTHOR]

Purpose: To investigate whether high power microwave could cause continuous disorders to learning and memory in Wistar rats and to explore the underlying mechanisms. Materials and methods: Eighty Wistar rats were exposed to a 2.856 GHz pulsed microwave source at a power density of 0 mW/cm2 and 50 mW/cm2 microwave for 6 min. The spatial memory ability, the structure of the hippocampus, contents of amino acids neurotransmitters in hippocampus and the expression of N-methyl-D-aspartic acid receptors (NMDAR) subunit 1, 2A and 2B (NR1, NR2A and NR2B) were detected at 1, 3, 6, 9, 12 and 18 months after microwave exposure. Results: Our results showed that the microwave-exposed rats showed consistent deficiencies in spatial learning and memory. The level of amino acid neurotransmitters also decreased after microwave radiation. The ratio of glutamate (Glu) and gammaaminobutyric acid (GABA) significantly decreased at 6 months. Besides, the hippocampus showed varying degrees of degeneration of neurons, increased postsynaptic density and blurred synaptic clefts in the exposure group. The NR1 and NR2B expression showed a significant decrease, especially the NR2B expression. Conclusions: This study indicated that the content of amino acids neurotransmitters, the expression of NMDAR subunits and the variation of hippocampal structure might contribute to the long-term cognitive impairment after microwave exposure. [ABSTRACT FROM AUTHOR]