Early exposure to intermediate-frequency magnetic fields alters brain biomarkers without histopathological changes in adult mice.
Recently we have reported that intermediate-frequency magnetic field (IF-MF) exposure transiently altered the mRNA expression levels of memory function-related genes in the hippocampi of adult male mice. However, the effects of IF-MF exposure during brain development on neurological biomarkers have not yet been clarified. In the present study, we investigated the effect of IF-MF exposure during development on neurological and immunological markers in the mouse hippocampus in 3- and 7-week-old male mice. Pregnant C57BL/6J mice were exposed to IF-MF (21 kHz, 3.8 mT) for one hour per day from organogenesis period day 7 to 17. At adolescence, some IF-MF-exposed mice were further divided into exposure, recovery, and sham-exposure groups. The adolescent-exposure groups were exposed again to IF-MF from postnatal day 27 to 48. The expression of mRNA in the hippocampi was examined using a real-time RT-PCR method, and microglia activation was examined by immunohistochemical analysis. The expression levels of NR1 and NR2B as well as transcription factors (CaMKIV, CREB1), inflammatory mediators (COX2, IL-1 b,TNF-α), and the oxidative stress marker heme-oxygenase (HO)-1 were significantly increased in the IF-MF-exposed mice, compared with the control group, in the 7-week-old mice, but not in the 3-week-old mice. Microglia activation was not different between the control and other groups. This study provides the first evidence that early exposure to IF-MF reversibly affects the NMDA receptor, its related signaling pathways, and inflammatory mediators in the hippocampus of young adult mice; these changes are transient and recover after termination of exposure without histopathological changes.
Center for Environmental Health Sciences, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan. tin.tin.win.shwe@nies.go.jp.
Tin-Tin
TT
Win-Shwe
Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako City, Saitama 351-0197, Japan. ohtani@niph.go.jp.
Shin
S
Ohtani
Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako City, Saitama 351-0197, Japan. ushiyama@niph.go.jp.
Akira
A
Ushiyama
Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako City, Saitama 351-0197, Japan. kunugita@niph.go.jp.
Naoki
N
Kunugita
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D054734:Calcium-Calmodulin-Dependent Protein Kinase Type 4 / Q000235:genetics; D017362:Cyclic AMP Response Element-Binding Protein / Q000235:genetics; D051546:Cyclooxygenase 2 / Q000235:genetics; D005260:Female; D051547:Heme Oxygenase-1 / Q000235:genetics; D006624:Hippocampus / Q000033:anatomy & histology / Q000378:metabolism*; D053583:Interleukin-1beta; D060526:Magnetic Fields / Q000009:adverse effects*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D015415:Biomarkers; C492004:Creb1 protein, mouse; D017362:Cyclic AMP Response Element-Binding Protein; C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D008565:Membrane Proteins; D012333:RNA, Messenger; D016194:Receptors, N-Methyl-D-Aspartate; D014409:Tumor Necrosis Factor-alpha; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D054734:Calcium-Calmodulin-Dependent Protein Kinase Type 4; C517685:Camk4 protein, mouse