Exposure to 50 Hz magnetic field modulates GABA A currents in cerebellar granule neurons through an EP receptor‐mediated PKC pathway

Previous work from both our lab and others have indicated that exposure to 50 Hz magnetic fields ( ELF ‐ MF ) was able to modify ion channel functions. However, very few studies have investigated the effects of MF on γ‐aminobutyric acid ( GABA ) type A receptors ( GABA A R s) channel functioning, which are fundamental to overall neuronal excitability. Here, our major goal is to reveal the potential effects of ELF ‐ MF on GABA A R s activity in rat cerebellar granule neurons ( CGN s). Our results indicated that exposing CGN s to 1 mT ELF ‐ MF for 60 min. significantly increased GABA A R currents without modifying sensitivity to GABA . However, activation of PKA by db‐ cAMP failed to do so, but led to a slight decrease instead. On the other hand, PKC activation or inhibition by PMA or Bis and Docosahexaenoic acid (DHA) mimicked or eliminated the field‐induced‐increase of GABA A R currents. Western blot analysis indicated that the intracellular levels of phosphorylated PKC ( pPKC ) were significantly elevated after 60 min. of ELF ‐ MF exposure, which was subsequently blocked by application of DHA or EP 1 receptor‐specific (prostaglandin E receptor 1) antagonist ( SC 19220), but not by EP 2‐ EP 4 receptor‐specific antagonists. SC 19220 also significantly inhibited the ELF ‐ MF ‐induced elevation on GABA A R currents. Together, these data obviously demonstrated for the first time that neuronal GABA A currents are significantly increased by ELF ‐ MF exposure, and also suggest that these effects are mediated via an EP 1 receptor‐mediated PKC pathway. Future work will focus on a more comprehensive analysis of the physiological and/or pathological consequences of these effects.