The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves
<b>Background</b>: Terahertz (THz) waves, lying between millimeter waves and infrared light, may interact with biomolecules due to their unique energy characteristics. However, whether THz waves are neurally regulated remains controversial, and the underlying mechanism is elusive. <b&...
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2025-04-01
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| author | Lequan Song Ji Dong Wenjing Cheng Zhengjie Fei Rui Wang Zhiwei He Junmiao Pan Li Zhao Hui Wang Ruiyun Peng |
| author_facet | Lequan Song Ji Dong Wenjing Cheng Zhengjie Fei Rui Wang Zhiwei He Junmiao Pan Li Zhao Hui Wang Ruiyun Peng |
| author_sort | Lequan Song |
| collection | DOAJ |
| description | <b>Background</b>: Terahertz (THz) waves, lying between millimeter waves and infrared light, may interact with biomolecules due to their unique energy characteristics. However, whether THz waves are neurally regulated remains controversial, and the underlying mechanism is elusive. <b>Methods</b>: Mouse brain slices were exposed to 1.94 THz waves for 1 h. Synaptic plasticity was evaluated via transmission electron microscopy (TEM), long-term potentiation (LTP), and neuronal class III β-tubulin (Tuj1) and synaptophysin (SYN) expression. Immunofluorescence (IF) and electrophysiology were used to identify neurons sensitive to THz waves. The calcium activity of excitatory neurons, glutamate receptor currents, and glutamate neuron marker expression was also assessed using calcium imaging, a patch clamp, and Western blotting (WB). Optogenetics and chemogenetics were used to determine the role of excitatory neurons in synaptic plasticity impairment after THz wave exposure. NMDA receptor 2B (GluN2B) was overexpressed in the ventral hippocampal CA1 (vCA1) by a lentivirus to clarify the role of GluN2B in THz wave-induced synaptic plasticity impairment. <b>Results</b>: Exposure to 1.94 THz waves increased postsynaptic density (PSD) thickness and reduced the field excitatory postsynaptic potential (fEPSP) slope and Tuj1 and SYN expression. THz waves diminished vCA1 glutamatergic neuron activity and excitability, neural electrical activity, and glutamate transporter function. THz waves reduced N-methyl-D-aspartate receptor (NMDAR) current amplitudes and NMDAR subunit expression. Activating vCA1 glutamatergic neurons through optogenetics and chemogenetics mitigated THz wave-induced synaptic plasticity impairment. GluN2B subunit overexpression improved synaptic plasticity marker expression, synaptic ultrastructure, and the fEPSP slope. <b>Conclusions</b>: Exposure to 1.94 THz waves decreased synaptic plasticity, glutamatergic neuron excitability, and glutamatergic synaptic transmission in the vCA1. Glutamatergic neuron activation and GluN2B overexpression alleviated THz wave-induced synaptic plasticity impairment; thus, neuromodulation could be a promising therapeutic strategy to mitigate the adverse effects of THz radiation. |
| format | Article |
| id | doaj-art-c59a60b47d184fd39bf19b5b6c06b003 |
| institution | DOAJ |
| issn | 2218-273X |
| language | English |
| publishDate | 2025-04-01 |
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| series | Biomolecules |
| spelling | doaj-art-c59a60b47d184fd39bf19b5b6c06b0032025-08-20T03:14:17ZengMDPI AGBiomolecules2218-273X2025-04-0115453210.3390/biom15040532The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz WavesLequan Song0Ji Dong1Wenjing Cheng2Zhengjie Fei3Rui Wang4Zhiwei He5Junmiao Pan6Li Zhao7Hui Wang8Ruiyun Peng9Beijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, ChinaBeijing Institute of Radiation Medicine, Beijing 100850, China<b>Background</b>: Terahertz (THz) waves, lying between millimeter waves and infrared light, may interact with biomolecules due to their unique energy characteristics. However, whether THz waves are neurally regulated remains controversial, and the underlying mechanism is elusive. <b>Methods</b>: Mouse brain slices were exposed to 1.94 THz waves for 1 h. Synaptic plasticity was evaluated via transmission electron microscopy (TEM), long-term potentiation (LTP), and neuronal class III β-tubulin (Tuj1) and synaptophysin (SYN) expression. Immunofluorescence (IF) and electrophysiology were used to identify neurons sensitive to THz waves. The calcium activity of excitatory neurons, glutamate receptor currents, and glutamate neuron marker expression was also assessed using calcium imaging, a patch clamp, and Western blotting (WB). Optogenetics and chemogenetics were used to determine the role of excitatory neurons in synaptic plasticity impairment after THz wave exposure. NMDA receptor 2B (GluN2B) was overexpressed in the ventral hippocampal CA1 (vCA1) by a lentivirus to clarify the role of GluN2B in THz wave-induced synaptic plasticity impairment. <b>Results</b>: Exposure to 1.94 THz waves increased postsynaptic density (PSD) thickness and reduced the field excitatory postsynaptic potential (fEPSP) slope and Tuj1 and SYN expression. THz waves diminished vCA1 glutamatergic neuron activity and excitability, neural electrical activity, and glutamate transporter function. THz waves reduced N-methyl-D-aspartate receptor (NMDAR) current amplitudes and NMDAR subunit expression. Activating vCA1 glutamatergic neurons through optogenetics and chemogenetics mitigated THz wave-induced synaptic plasticity impairment. GluN2B subunit overexpression improved synaptic plasticity marker expression, synaptic ultrastructure, and the fEPSP slope. <b>Conclusions</b>: Exposure to 1.94 THz waves decreased synaptic plasticity, glutamatergic neuron excitability, and glutamatergic synaptic transmission in the vCA1. Glutamatergic neuron activation and GluN2B overexpression alleviated THz wave-induced synaptic plasticity impairment; thus, neuromodulation could be a promising therapeutic strategy to mitigate the adverse effects of THz radiation.https://www.mdpi.com/2218-273X/15/4/532terahertzbrain slicesynaptic plasticityglutamatergic neuronsLTPGluN2B |
| spellingShingle | Lequan Song Ji Dong Wenjing Cheng Zhengjie Fei Rui Wang Zhiwei He Junmiao Pan Li Zhao Hui Wang Ruiyun Peng The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves Biomolecules terahertz brain slice synaptic plasticity glutamatergic neurons LTP GluN2B |
| title | The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves |
| title_full | The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves |
| title_fullStr | The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves |
| title_full_unstemmed | The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves |
| title_short | The Role of Glutamatergic Neurons in Changes of Synaptic Plasticity Induced by THz Waves |
| title_sort | role of glutamatergic neurons in changes of synaptic plasticity induced by thz waves |
| topic | terahertz brain slice synaptic plasticity glutamatergic neurons LTP GluN2B |
| url | https://www.mdpi.com/2218-273X/15/4/532 |
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