Extremely low-freauency electromagnetic fields promote in vitro neurogenesis via upregulation of Cav1-channel activity

Roberto Piacentini, Cristian Ripoli, Daniele Mezzogori, Gian Battista Azzena, Claudio Grassi

Research output: Contribution to journalArticle

Abstract

We previously reported that exposure to extremely low-frequency electromagnetic fields (ELFEFs) increases the expression and function of voltage-gated Ca2+ channels and that Ca2+ influx through Cav1 channels plays a key role in promoting the neuronal differentiation of neural stem/progenitor cells (NSCs). The present study was conducted to determine whether ELFEFs influence the neuronal differentiation of NSCs isolated from the brain cortices of newborn mice by modulating Ca v1-channel function. In cultures of differentiating NSCs exposed to ELFEFs (1 mT, 50 Hz), the percentage of cells displaying immunoreactivity for neuronal markers (β-111-tubulin, MAP2) and for Cav1.2 and Cav1.3 channels was markedly increased. NSC-differentiated neurons in ELFEF-exposed cultures also exhibited significant increases in spontaneous firing, in the percentage of cells exhibiting Ca2+ transients in response to KCI stimulation, in the amplitude of these transients and of Ca 2+ currents generated by the activation of Cav1 channels. When the Cav1-channel blocker nifedipine (5 μM) was added to the culture medium, the neuronal yield of NSC differentiation dropped significantly, and ELFEF exposure no longer produced significant increases in β-III-tubulin- and MAP2-immunoreactivity rates. In contrast, the effects of ELFEFs were preserved when NSCs were cultured in the presence of either glutamate receptor antagonists or Cav2.1- and Cav2.2- channel blockers. ELFEF stimulation during the first 24 h of differentiation caused Cav1-dependent increases in the number of cells displaying CREB phosphorylation. Our data suggest that ELFEF exposure promotes neuronal differentiation of NSCs by upregulating Cav1-channel expression and function.

Original languageEnglish
Pages (from-to)129-139
Number of pages11
JournalJournal of Cellular Physiology
Volume215
Issue number1
DOIs
Publication statusPublished - Apr 2008

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ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

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