Study type: Medical/biological study (experimental study)

Extremely low-frequency electromagnetic fields promote in vitro neurogenesis via upregulation of Ca(v)1-channel activity. med./bio.

Published in: J Cell Physiol 2008; 215 (1): 129-139

Aim of study (acc. to author)

To study whether extremely low frequency electromagnetic fields influence the neuronal differentiation of neural stem cells/progenitor cells isolated from the brain cortices of newborn mice and, if so, whether this effect is mediated by changes in intracellular Ca2+ signaling.

Background/further details

To study the effects of Ca2+ signals across cell membrane on neuronal differentiation, the following compounds were added to the culture medium: the selective calcium channel (Cav1)-blocker, nifedipine; the nonselective calcium channel (Cav2.2 and Cav2.1)-blocker, v-conotoxin MVIIC; a mixture of the Ca2+ permeable ionotropic glutamate receptor antagonists CNQX and D-AP5.

Endpoint

Exposure

Exposure Parameters
Exposure 1: 50 Hz
Exposure duration: continuous for up to 12 days

Exposure 1

Main characteristics
Frequency 50 Hz
Type
Exposure duration continuous for up to 12 days
Exposure setup
Exposure source
Setup solenoid placed inside a CO2 incubator
Parameters
Measurand Value Type Method Mass Remarks
magnetic flux density 1 mT - - - -

Reference articles

  • Wolf FI et al. (2005): 50-Hz extremely low frequency electromagnetic fields enhance cell proliferation and DNA damage: possible involvement of a redox mechanism.
  • Grassi C et al. (2004): Effects of 50 Hz electromagnetic fields on voltage-gated Ca2+ channels and their role in modulation of neuroendocrine cell proliferation and death.

Exposed system:

Methods Endpoint/measurement parameters/methodology

Investigated system:
Time of investigation:
  • after exposure

Main outcome of study (acc. to author)

The data demonstrated that the neuronal yield of neural stem cell/progenitor cell differentiation was significantly increased by extremely low frequency electromagnetic field stimulation and that this effect is dependent on exposure-induced upregulation of calcium channel (Cav1) expression and activity.

Study character:

Study funded by

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