The Study Of The Effect And Mechanism Of Extremely Low-frequency Electromagnetic Fields On T-type Calcium Channels

Electromagnetic fields (EMFs) are the kind of fields that transport in the form of photons, they include geomagnetic field, EMFs generated by electric appliances used in daily life, radio wave, X-ray, y-ray and cosmic rays. As we are now increasingly subjected EMFs emitted from electric appliances like cell phone, Wi-Fi, and wearable gadgets like Google Glass, the public are more than ever concerned about the adverse effects of EMFs. The well recognized effects of EMFs are generally divided into a category of two:thermal effects, with the extensive use of microwave as an example, and nonthermal effects, which has stayed controversial till this day. The existence of nonthermal effects of high frequency EMFs are beyond argument, but scientists are still puzzled by how extremely low frequency electromagnetic fields (ELF-EMFs) are able to cause nonthermal effects.As the methodologies that are available grows and more resources are devoted to this area, scientists are getting closer to the mechanisms behind the biological effects of EMFs.EMFs causes various biological effects through altering intracellular calcium homeostasis. Recent studies have indicated voltage gated calcium channels as the direct target of EMFs, and the role of high voltage-gated (HVA) calcium channels in EMFs, more specifically ELF-EMFs induced effects have been extensively studied. However, the effect of ELF-EMF on low-voltage-gated (LVA) T-type calcium channels has not been reported. In this study, we test the effect of ELF-EMF (50 Hz) on human T-type calcium channels transfected in HEK293 cells. Conversely to its stimulant effects on HVA channels, ELF-EMF exposure inhibited all T-type (Cav3.1, Cav3.2 and Cav3.3) channels, preferentially Cav3.2 in a time dependent manner. Neither the protein expression nor the steady-state activation and inactivation kinetics of Cav3.2 channels were altered by ELF-EMF (50Hz,0.2mT) exposure. Exposure to ELF-EMF increased both arachidonic acid (AA) and leukotriene E4 (LTE4) levels in HEK293 cells. CAY10502 and bestatin, which block the increase of AA and LTE4 respectively, abrogated the ELF-EMF inhibitory effect on Cav3.2 channels. Exogenous LTE4 mimicked the ELF-EMF inhibition of T-type calcium channels. ELF-EMF (50 Hz) inhibits native T-type calcium channels in primary cultured mouse cortical neurons via LTE4. We conclude that 50 Hz ELF-EMF inhibits T-type calcium channels through AA/LTE4 signaling pathway.