Effects of 50 Hz electromagnetic fields on voltage-gated Ca2+ channels and their role in modulation of neuroendocrine cell proliferation and death

Possible correlation between the effects of electromagnetic fields (EFs) on voltage-gated Ca2+ channels, cell proliferation and apoptosis was investigated in neural and neurcendocrine cells. Exposure to 50 Hz EFs significantly enhanced proliferation in human neuroblastoma IMR32 (+40%) and rat pituitary GH3 cells (+38%). In IMR32 cells EF stimulation also inhibited puromycin- and H2O2-induced apoptosis (-22 and -33%, respectively). EF effects on proliferation and apoptosis were counteracted by Ca2+ channel blockade. In whole-cell patch-clamp experiments 24-72 h exposure to EFs increased macroscopic Ba2+-current density in both GH3 (+67%) and IMR32 cells (+40%). Single-channel recordings showed that gating of L and N channels was instead unaffected, thus suggesting that the observed enhancement of current density was due to increased number of voltage-gated Ca2+ channels. Western blot analysis of plasma membrane-enriched microsomal fractions of GH3 and IMR32 cells confirmed enhanced expression of Ca2+ channel subunit alpha(1) following exposure to EFs. These data provide the first direct evidence that EFs enhance the expression of voltage-gated Ca2+ channels on plasma membrane of the exposed cells. The consequent increase in Ca2+ influx is likely responsible for the EF-induced modulation of neuronal cell proliferation and apoptosis. (C) 2003 Elsevier Ltd. All rights reserved.