AbstractPrevious 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 ofMFon γ‐aminobutyric acid (GABA) type A receptors (GABAARs) channel functioning, which are fundamental to overall neuronal excitability. Here, our major goal is to reveal the potential effects ofELF‐MFonGABAARs activity in rat cerebellar granule neurons (CGNs). Our results indicated that exposingCGNs to 1 mTELF‐MFfor 60 min. significantly increasedGABAARcurrents without modifying sensitivity toGABA. However, activation ofPKAby db‐cAMPfailed to do so, but led to a slight decrease instead. On the other hand,PKCactivation or inhibition byPMAor Bis and Docosahexaenoic acid (DHA) mimicked or eliminated the field‐induced‐increase ofGABAARcurrents. Western blot analysis indicated that the intracellular levels of phosphorylatedPKC(pPKC) were significantly elevated after 60 min. ofELF‐MFexposure, which was subsequently blocked by application ofDHAorEP1 receptor‐specific (prostaglandin E receptor 1) antagonist (SC19220), but not byEP2‐EP4 receptor‐specific antagonists.SC19220 also significantly inhibited theELF‐MF‐induced elevation onGABAARcurrents. Together, these data obviously demonstrated for the first time that neuronalGABAAcurrents are significantly increased byELF‐MFexposure, and also suggest that these effects are mediatedviaanEP1 receptor‐mediatedPKCpathway. Future work will focus on a more comprehensive analysis of the physiological and/or pathological consequences of these effects.