Saito Atsushi, Takahashi Masayuki, Makino Kei, Suzuki Yukihisa, Jimbo Yasuhiko, Nakasono Satoshi
Biological Environment Sector, Environmental Science Research Laboratory, Central Research Institute of Electric Power Industry, Chiba, Japan.
Department of Electrical and Electronic Engineering, Graduate School of Science and Engineering, Tokyo Metropolitan University, Tokyo, Japan.
Front Physiol. 2018 Mar 12;9:189. doi: 10.3389/fphys.2018.00189. eCollection 2018.
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 (-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 (-field: >0.3 V/m), and the response was due to reduced inhibitory pacemaker-like neuronal activity.
高强度和低频（1 - 100千赫兹）的时变电磁场通过刺激神经系统来作用于人体。在工频范围（50/60赫兹）内，国际指南将培养的神经网络中外部电场诱导的神经元调制的频率依赖性阈值用作生物学指标之一；然而，磁场诱导的神经元调制阈值尚未阐明。在本研究中，我们将源自大鼠脑的神经网络暴露于高强度工频磁场（hPF - MF），并使用基于多电极阵列（MEA）的细胞外记录技术评估同步爆发活动的调制情况。短期暴露于hPF - MF（均方根（rms）为50 - 400毫特斯拉，50赫兹，正弦波，6秒）后，400毫特斯拉暴露组的同步爆发活动增加。另一方面，50 - 200毫特斯拉暴露组未观察到变化。为了阐明400毫特斯拉hPF - MF暴露诱导神经元反应的机制，我们在使用甲基荷包牡丹碱（BMI）阻断抑制性突触后对其进行评估；随后，应用BMI后观察到爆发活动增加，且400毫特斯拉hPF - MF暴露的反应消失。因此，提示hPF - MF暴露的反应与抑制性输入有关。接下来，我们通过应用CNQX和D - AP5筛选出显示自主4 - 10赫兹放电的抑制性起搏器样神经元活动，并证实400毫特斯拉hPF - MF暴露后该活动减少。将这些实验结果与培养基中感应电场（-场）的估计值进行比较发现，同步爆发活动的变化发生在超过0.3伏/米时，这与先前使用外部电场的研究结果相当。此外，结果表明400毫特斯拉hPF - MF暴露后神经元活动的增强与起搏器样神经元自主活动的抑制有关。我们的结果表明，hPF - MF暴露（-场：>0.3伏/米）会增加同步爆发活动，且该反应是由于抑制性起搏器样神经元活动减少所致。
