%A Saito,Atsushi %A Takahashi,Masayuki %A Makino,Kei %A Suzuki,Yukihisa %A Jimbo,Yasuhiko %A Nakasono,Satoshi %D 2018 %J Frontiers in Physiology %C %F %G English %K Power frequency magnetic field,neuronal network,synchronized bursting activity,Multi-Electrode Array,pacemaker-like neuron,inhibitory synapse %Q %R 10.3389/fphys.2018.00189 %W %L %M %P %7 %8 2018-March-12 %9 Original Research %+ Atsushi Saito,Biological Environment Sector, Environmental Science Research Laboratory, Central Research Institute of Electric Power Industry,Japan,saito@criepi.denken.or.jp %# %! Response to magnetic field exposure %* %< %T Response of Cultured Neuronal Network Activity After High-Intensity Power Frequency Magnetic Field Exposure %U https://www.frontiersin.org/articles/10.3389/fphys.2018.00189 %V 9 %0 JOURNAL ARTICLE %@ 1664-042X %X High-intensity and low frequency (1–100 kHz) time-varying electromagnetic fields stimulate the human body through excitation of the nervous system. In power frequency range (50/60 Hz), a frequency-dependent threshold of the external electric field-induced neuronal modulation in cultured neuronal networks was used as one of the biological indicator in international guidelines; however, the threshold of the magnetic field-induced neuronal modulation has not been elucidated. In this study, we exposed rat brain-derived neuronal networks to a high-intensity power frequency magnetic field (hPF-MF), and evaluated the modulation of synchronized bursting activity using a multi-electrode array (MEA)-based extracellular recording technique. As a result of short-term hPF-MF exposure (50–400 mT root-mean-square (rms), 50 Hz, sinusoidal wave, 6 s), the synchronized bursting activity was increased in the 400 mT-exposed group. On the other hand, no change was observed in the 50–200 mT-exposed groups. In order to clarify the mechanisms of the 400 mT hPF-MF exposure-induced neuronal response, we evaluated it after blocking inhibitory synapses using bicuculline methiodide (BMI); subsequently, increase in bursting activity was observed with BMI application, and the response of 400 mT hPF-MF exposure disappeared. Therefore, it was suggested that the response of hPF-MF exposure was involved in the inhibitory input. Next, we screened the inhibitory pacemaker-like neuronal activity which showed autonomous 4–10 Hz firing with CNQX and D-AP5 application, and it was confirmed that the activity was reduced after 400 mT hPF-MF exposure. Comparison of these experimental results with estimated values of the induced electric field (E-field) in the culture medium revealed that the change in synchronized bursting activity occurred over 0.3 V/m, which was equivalent to the findings of a previous study that used the external electric fields. In addition, the results suggested that the potentiation of neuronal activity after 400 mT hPF-MF exposure was related to the depression of autonomous activity of pacemaker-like neurons. Our results indicated that the synchronized bursting activity was increased by hPF-MF exposure (E-field: >0.3 V/m), and the response was due to reduced inhibitory pacemaker-like neuronal activity.