Pulsed magnetic fields modulate neuronal primary metabolites in vitro
Hong, I., Maker, G., Mullaney, I., Garrett, A., Rodger, J. and Etherington, S. (2014) Pulsed magnetic fields modulate neuronal primary metabolites in vitro. In: Meeting of the Australasian Neuroscience Society, 28 - 31 January, Adelaide, SA, Australia.
Pulsed Magnetic Fields (PMFs) are currently being used to treat a range of neurological conditions such as depression. However, little is known about the cellular mechanisms behind their therapeutic effects.
To investigate the influence of PMFs on neuronal biochemical processes.
B50 rat neuroblastoma cells were seeded on to 6-well plates, grown to confluence and stimulated with PMFs (~10 mT) at 1 or 10 Hz for 10 minutes (controls were unstimulated). Cells were immediately quenched post-stimulation with ice-cold PBS and then freeze-dried. Cells were subsequently lysed, derivatised and analysed using untargeted gas chromatography-mass spectrometry (GC-MS).
Initial principal component analysis revealed 3 distinct groups (control, 1 and 10 Hz). Significant differences were found in 12 metabolites (PMF stimulated vs unstimulated controls, ANOVA, n= 4-6). PMF stimulated cells had significantly lower levels (p≤0.05) of GABA precursors (succinate, aspartate, proline and glutamate). These changes may be due to increased inhibitory neurotransmitter release during PMF stimulation. Two metabolites involved in calcium signaling (inositol and serine) were also significantly lower in PMF treated cells. In addition, PMF stimulation at 1Hz reduced metabolite levels to a greater extent than 10 Hz, an effect which reached significance for glycine (p≤0.05).
PMFs at either 1 or 10 Hz significantly reduced intracellular metabolites involved with inhibitory neurotransmission and calcium signaling in neuronal cell cultures. The changes to neuronal metabolism were frequency dependent. Our data suggest that acute PMF stimulation induce biochemical changes that may modulate inhibitory neurotransmission and calcium signaling.
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