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      RF-EMF 노출이 생쥐 대뇌 피질에서 UBE3A, NMDA 수용체 발현 및 CREB-GSK3β 경로 활성화에 미치는 영향

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      https://www.riss.kr/link?id=T17411198

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      다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

      The recent increase in the use of wireless communication devices has led to a rapid increase in our daily exposure to radiofrequency electromagnetic fields (RF-EMFS). There are numerous studies reporting that excessive exposure to RF-EMF can affect the brain and nervous system. In particular, there have been reports of impaired synapse formation in young mice exposed to RF-EMF, potentially leading to neurodevelopmental and functional decline. Synapse formation is particularly crucial for growing children. Therefore, this study aimed to elucidate the effects of RF-EMF exposure on nervous system function, particularly synaptic function in the cerebral cortex. We hypothesized that four weeks of exposure to radiofrequency electromagnetic fields (1850 MHz RF-EMF) (4 W/kg, 5 h/day) could alter synaptic structure and function, as well as neurotransmitters, leading to neural circuit disruption. In this process, we identified changes in the N-methyl-D-aspartate receptor (NMDAR), a key protein involved in synapse formation. Ubiquitination ligase E3 (UBE3A) plays a crucial role in nervous system development and function, regulating synaptic strength and stability through the degradation and relocation of synaptic target proteins. In particular, overexpression or deficiency of UBE3A has been reported to be closely associated with neurodevelopmental disorders such as Angelman syndrome and autism spectrum disorders such as Dup 15q syndrome. Therefore, this study exposed young mice to 1850 MHz radiofrequency electromagnetic fields for 4 weeks after birth and observed synaptic changes in the cerebral cortex. We identified that RF-EMF exposure affects neural development by inducing UBE3A overexpression. This decreased NMDAR expression, which in turn reduced levels of the synaptic cell adhesion molecule Neuroxin-1a gene. This, in turn, affected CREB and GSK3β phosphorylation, which are essential for neuronal signaling, rleading to abnormalities in nesting behavior, a vital survival behavior in young mice. This suggests the possibility that exposure to radiofrequency electromagnetic fields (1850 MHz RF-EMF (4 W/kg, 5 h/day) for 4 weeks in young mice may cause functional changes due to instability in synapse formation.
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      The recent increase in the use of wireless communication devices has led to a rapid increase in our daily exposure to radiofrequency electromagnetic fields (RF-EMFS). There are numerous studies reporting that excessive exposure to RF-EMF can affect th...

      The recent increase in the use of wireless communication devices has led to a rapid increase in our daily exposure to radiofrequency electromagnetic fields (RF-EMFS). There are numerous studies reporting that excessive exposure to RF-EMF can affect the brain and nervous system. In particular, there have been reports of impaired synapse formation in young mice exposed to RF-EMF, potentially leading to neurodevelopmental and functional decline. Synapse formation is particularly crucial for growing children. Therefore, this study aimed to elucidate the effects of RF-EMF exposure on nervous system function, particularly synaptic function in the cerebral cortex. We hypothesized that four weeks of exposure to radiofrequency electromagnetic fields (1850 MHz RF-EMF) (4 W/kg, 5 h/day) could alter synaptic structure and function, as well as neurotransmitters, leading to neural circuit disruption. In this process, we identified changes in the N-methyl-D-aspartate receptor (NMDAR), a key protein involved in synapse formation. Ubiquitination ligase E3 (UBE3A) plays a crucial role in nervous system development and function, regulating synaptic strength and stability through the degradation and relocation of synaptic target proteins. In particular, overexpression or deficiency of UBE3A has been reported to be closely associated with neurodevelopmental disorders such as Angelman syndrome and autism spectrum disorders such as Dup 15q syndrome. Therefore, this study exposed young mice to 1850 MHz radiofrequency electromagnetic fields for 4 weeks after birth and observed synaptic changes in the cerebral cortex. We identified that RF-EMF exposure affects neural development by inducing UBE3A overexpression. This decreased NMDAR expression, which in turn reduced levels of the synaptic cell adhesion molecule Neuroxin-1a gene. This, in turn, affected CREB and GSK3β phosphorylation, which are essential for neuronal signaling, rleading to abnormalities in nesting behavior, a vital survival behavior in young mice. This suggests the possibility that exposure to radiofrequency electromagnetic fields (1850 MHz RF-EMF (4 W/kg, 5 h/day) for 4 weeks in young mice may cause functional changes due to instability in synapse formation.

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      목차 (Table of Contents)

      • Ⅰ. Introduction 1
      • Ⅱ. Material and Method 3
      • 2.1 Animals 3
      • 2.2 RF-EMF Exposure in mic 3
      • 2.3 Mouse Valproic acid( 2-propyl-pentanoc acid; VPA) injection 3
      • Ⅰ. Introduction 1
      • Ⅱ. Material and Method 3
      • 2.1 Animals 3
      • 2.2 RF-EMF Exposure in mic 3
      • 2.3 Mouse Valproic acid( 2-propyl-pentanoc acid; VPA) injection 3
      • 2.4 Mouse Cortex RNA purification 3
      • 2.5 Mouse behavior TEST 4
      • 2.6 RT-PCR 4
      • 2.7 Western bloting 5
      • 2.8 Statistical analysis 5
      • Ⅲ. Result 6
      • 3.1 Changes in brain-to-body weight ratio across developmental stages 7
      • 3.2 Effects of RF-EMF and VPA exposure on nest-building behavior 9
      • 3.3 Social Interaction Analysis in RF-EMF–Exposed and VPA-Treated Mice 11
      • 3.4 Alterations in UBE3A Protein Expression Following Exposure to RF-EMF or valproic acid 13
      • 3.5Alterations in NMDA Receptor Expression Following Exposure to RF-EMF or valproic acid 15
      • 3.6 Effects of RF-EMF Exposure and VPA Treatment on Synapse Formation Related Genes 17
      • 3.7 Effects of RF-EMF exposure or valproic acid treatment on synaptic and intracellular signaling proteins in the mouse cerebral cortex 19
      • Ⅳ. Discussion 20
      • V. Conclusion 26
      • Ⅵ. Reference 28
      • 외국어초록 37
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