Microwave-Induced Structural and Functional Injury of Hippocampal and PC12 Cells Is Accompanied by Abnormal Changes in the NMDAR-PSD95-CaMKII Pathway

Wang, Lifeng; Li, Wei; Qiao, Si-Mo; Gao, Xiao-Na; Gao, Yabing; Wang, Shuiming; Zhao, Li; Dong, Ji; Xu, Xinping; Zhou, Hongmei; Hu, Xiaoyun; Peng, Ruiyun

doi:10.1159/000398803

Cited by 15 publications

(12 citation statements)

References 38 publications

(34 reference statements)

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“…Significant and immediate effects on the binding parameters (Kd and Bmax) of NMDARs were found after acute exposure to 900 MHz electromagnetic fields [8]. Abnormal protein and mRNA expression, as well as posttranslational modifications, were detected in the NMDAR-PSD95-CaMKII pathway after microwave exposure, and a GluN2B subunit gene promoter region variant was associated with microwave-induced neuron impairment [31,32]. However, further studies on hippocampal neurons regarding the effects of microwave exposure on NMDAR subunits and activity have been limited.…”

Section: Discussionmentioning

confidence: 99%

“…Wang LF [31] detected abnormal protein and mRNA expression, as well as posttranslational modifications, in the NMDAR-PSD95-CaMKII pathway and its associated components, such as synapsin I, following the microwave radiation exposure of rats and PC12 cells. In another study, a novel rat GluN2B subunit gene promoter region variant was associated with microwave-induced neuron impairment [32].…”

Section: Discussionmentioning

confidence: 99%

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Protective Role of NMDAR for Microwave-Induced Synaptic Plasticity Injuries in Primary Hippocampal Neurons

Wang¹,

Tan²,

Zhao³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The N-methyl-D-aspartic acid receptor (NMDAR) has been extensively studied for its important roles in synaptic plasticity and learning and memory. However, the effects of microwave radiation on the subunit composition and activity of NMDARs and the relationship between NMDARs and microwave-induced synaptic plasticity have not been thoroughly elucidated to date. Materials: In our study, primary hippocampal neurons were used to evaluate the effects of microwave radiation on synaptic plasticity. Structural changes were observed by diolistic (Dil) labeling and scanning electron microscopy (SEM) observation. Functional synaptic plasticity was reflected by the NMDAR currents, which were detected by whole cell patch clamp. We also detected the expression of NMDAR subunits by real-time PCR and Western blot analysis. To clarify the effects of microwave radiation on NMDAR-induced synaptic plasticity, suitable agonists or inhibitors were added to confirm the role of NMDARs on microwave-induced synaptic plasticity. Dil labeling, SEM observation, whole cell patch clamp, real-time PCR and Western blot analysis were used to evaluate changes in synaptic plasticity after treatment with agonists or inhibitors. Results: Our results found that microwave exposure impaired neurite development and decreased mRNA and protein levels and the current density of NMDARs. Due to the decreased expression of NMDAR subunits after microwave exposure, the selective agonist NMDA was added to identify the role of NMDARs on microwave-induced synaptic plasticity injuries. After adding the agonist, the expression of NMDAR subunits recovered to the normal levels. In addition, the microwave-induced structural and functional synaptic plasticity injuries recovered, including the number and length of neurites, the connections between neurons, and the NMDAR current. Conclusion: Microwave radiation caused neuronal synaptic plasticity injuries in primary hippocampal neurons, and NMDARs played protective roles on the damage process.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective Role of NMDAR for Microwave-Induced Synaptic Plasticity Injuries in Primary Hippocampal Neurons

Wang¹,

Tan²,

Zhao³

et al. 2018

Cell Physiol Biochem

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“…6 The protein kinase A (PKA)/Ca 2þ -calmodulin dependent kinase (CaMK) IV could phosphorylate Ser9 of site one that is shared by all the synapsins in the N-terminal domain A. 6,[16][17][18] The Ser9 phosphorylation regulates neurite elongation and SV mobilization, which has a prominent role in the expression of posttetanic potentiation and short-term synaptic enhancement. 19 In addition, a nonhydrolysable analog of plateletactivating factor (PAF) enhances LTP and promotes learning and memory through increasing synapsin-I phosphorylation at sites one (PKA and CaMKI/IV) and three (CaMKII) that is associated with decreased binding of synapsin-I to SV or actin and increased neurotransmitter release.…”

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confidence: 99%

“…19 In addition, a nonhydrolysable analog of plateletactivating factor (PAF) enhances LTP and promotes learning and memory through increasing synapsin-I phosphorylation at sites one (PKA and CaMKI/IV) and three (CaMKII) that is associated with decreased binding of synapsin-I to SV or actin and increased neurotransmitter release. 18,20 The underlying mechanism involves elevated Ca 2þ within presynaptic boutons and PKC activation. 21 Synapsin-I also contained multiple consensus sites four to six for extracellular signal-regulated kinase 1/2 (ERK1/2) and cyclin-dependent kinase 1/5 (CDK1/5), and the phosphorylation at these sites contributes to release neurotransmitters.…”

mentioning

confidence: 99%

“…21 Synapsin-I also contained multiple consensus sites four to six for extracellular signal-regulated kinase 1/2 (ERK1/2) and cyclin-dependent kinase 1/5 (CDK1/5), and the phosphorylation at these sites contributes to release neurotransmitters. 6,16,18 The conventional Ca 2þ -activated, phospholipid-dependent protein kinase C (cPKC) belongs to serine/threonine protein kinase family. 22,23 The cPKCc, one of the PKC family Copyright 2019 The Authors iovs.arvojournals.org j ISSN: 1552-5783 members, is neuron-specific and only expressed in neurons of cerebral cortex and spinal cord.…”

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confidence: 99%

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Modulation of cPKCγ on Synapsin-Ia/b–Specific Phosphorylation Sites in the Developing Visual Cortex of Mice

Wang

Ding

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To explore the role of synapsin-Ia/b in visual cortical plasticity, the dynamic changes in total protein expression (T-) and conventional protein kinase C (cPKC)c-modulated phosphorylation (P-) levels of synapsin-Ia/b were observed in the developing visual cortex of mice. METHODS. The Western blot analysis was used to determine the levels of T-and P-synapsin-Ia/b at site of Ser9, 549, and 603; the cPKCc gene wild-type (cPKCc þ/þ) and knockout (cPKCc À/À) mice were applied to explore the modulation of cPKCc on synapsin-Ia/b phosphorylation status in visual cortex of mice at postnatal 7 to 60 days (P7-P60, n ¼ 6 per group). RESULTS. The results showed that T-synapsin-Ia/b protein levels significantly increased at P14 to P35 and peaked at P42 to 60 (P < 0.001) in visual cortex when compared with that of P7 cPKCc þ/þ mice, and cPKCc À/À did not affect this pattern of T-synapsin-Ia/b protein expressions. For synapsin-Ia/b phosphorylation status, the levels of P-Ser9 and 603 synapsin-Ia/b significantly elevated at P21 to P28 (P < 0.05 or 0.001), and then went down and maintained at lower levels at P35 to P60 (P < 0.05 or 0.001) compared with P7 cPKCc þ/þ mice. In addition, the cPKCc gene knockout could significantly (P < 0.001) inhibit both the increase and decrease of P-Ser9 and 603 synapsin-Ia/b levels when compared with cPKCc þ/þ mice at P7 to P60. However, there were no significant changes of P-Ser549 synapsin-Ia/b in the developing visual cortex of both cPKCc þ/þ and cPKCc À/À mice at P7 to P60. CONCLUSIONS. These results suggested that both protein expression levels and cPKCcmodulated phosphorylation status at Ser9 and 603 of synapsin-Ia/b may play important role in developing visual cortex of mice.

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Effects of Nonthermal Radiofrequency Stimulation on Neuronal Activity and Neural Circuit in Mice

Hao¹,

Liu

et al. 2023

Advanced Science

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Whether the nonthermal effects of radiofrequency radiation (RFR) exist and how nonthermal RFR acts on the nervous system are unknown. An animal model of spatial memory impairment is established by exposing mice to 2856-MHz RFR in the range of thermal noise (≤1 °C). Glutamate release in the dorsal hippocampus (dHPC) CA1 region is not significantly changed after radiofrequency exposure, whereas dopamine release is reduced. Importantly, RFR enhances glutamatergic CA1 pyramidal neuron calcium activity by nonthermal mechanisms, which recover to the basal level with RFR termination. Furthermore, suppressed dHPC dopamine release induced by radiofrequency exposure is due to decreased density of dopaminergic projections from the locus coeruleus to dHPC, and artificial activation of dopamine axon terminals or D1 receptors in dHPC CA1 improve memory damage in mice exposed to RFR. These findings indicate that nonthermal radiofrequency stimulation modulates ongoing neuronal activity and affects nervous system function at the neural circuit level.

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Microwave-Induced Structural and Functional Injury of Hippocampal and PC12 Cells Is Accompanied by Abnormal Changes in the NMDAR-PSD95-CaMKII Pathway

Cited by 15 publications

References 38 publications

Protective Role of NMDAR for Microwave-Induced Synaptic Plasticity Injuries in Primary Hippocampal Neurons

Protective Role of NMDAR for Microwave-Induced Synaptic Plasticity Injuries in Primary Hippocampal Neurons

Modulation of cPKCγ on Synapsin-Ia/b–Specific Phosphorylation Sites in the Developing Visual Cortex of Mice

Effects of Nonthermal Radiofrequency Stimulation on Neuronal Activity and Neural Circuit in Mice

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