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Although the modulation of Ca 2+  channel activity by extremely low-frequency electromagnetic fields (ELF-EMF) has been studied previously, few reports have addressed the effects of such fields on the activity of voltage-activated Na +  channels (Na v ). Here, we investigated the effects of ELF-EMF on Na v  activity in rat cerebellar granule cells (GCs). Our results reveal that exposing cerebellar GCs to ELF-EMF for 10–60 min significantly increased Na v  currents ( I   Na ) by 30–125% in a time- and intensity-dependent manner. The Na v  channel steady-state activation curve, but not the steady-state inactivation curve, was significantly shifted (by 5.2 mV) towards hyperpolarization by ELF-EMF stimulation. This phenomenon is similar to the effect of intracellular application of arachidonic acid (AA) and prostaglandin E 2  (PGE 2 ) on  I   Na  in cerebellar GCs. Increases in intracellular AA, PGE 2  and phosphorylated PKA levels in cerebellar GCs were observed following ELF-EMF exposure. Western blottings indicated that the Na V  1.2 protein on the cerebellar GCs membrane was increased, the total expression levels of Na V  1.2 protein were not affected after exposure to ELF-EMF. Cyclooxygenase inhibitors and PGE 2  receptor (EP) antagonists were able to eliminate this ELF-EMF-induced increase in phosphorylated PKA and  I   Na . In addition, ELF-EMF exposure significantly enhanced the activity of PLA 2  in cerebellar GCs but did not affect COX-1 or COX-2 activity. Together, these data demonstrate for the first time that neuronal  I   Na  is significantly increased by ELF-EMF exposure  via  a cPLA2 AA PGE 2  EP receptors PKA signaling pathway.

plos one

Exposure to Extremely Low-Frequency Electromagnetic Fields Modulates Na+ Currents in Rat Cerebellar Granule Cells through Increase of AA/PGE2 and EP Receptor-Mediated cAMP/PKA Pathway