• mitogen-activated protein kinase (MAPK);
  • primary cultured cortical neurons (PCNs);
  • extra-cellular-regulated kinase (ERK);
  • and c-Jun N-terminal kinase (JNK)


Intense uniform magnetic fields, such as those used in magnetic resonance imaging (MRI), are thought to exert little influence at the cellular level. Here we report modifications of the signaling cascades in rat cortical neurons cultured for 1 h in magnetic fields of up to 5 Tesla. The activation of c-Jun N-terminal kinase (JNK) increases monotonically with field strength, with a maximal activation of ∼10% at 5 T, whereas the activation of extra cellular-regulated kinase (ERK) shows a maximum at 0.75 T (∼10%). Since ERK is involved in cellular differentiation, these results indicate a magnetic induction of the signaling events associated with differentiation. However, the cells respond to further increases in field strength by evoking a stress response, since JNK is a stress-activated protein kinase. Three possible mechanisms are discussed and of these, the most plausible is magnetic field induced change in the membrane rest potential, a microscale magnetohydrodynamic effect. This mechanism most likely involves the activation of voltage dependent Ca2+ channel opening; since intracellular Ca2+ concentration was also found to be modified by the static magnetic field. Bioelectromagnetics 27:35–42, 2006. © 2005 Wiley-Liss, Inc.