Effect of a 0.5-T static magnetic field on conduction in guinea pig spinal cord

doi:10.1016/j.jns.2004.04.010

Journal of the Neurological Sciences

Volume 222, Issues 1–2, 15 July 2004, Pages 55-57

https://doi.org/10.1016/j.jns.2004.04.010 Get rights and content

Abstract

Compound-evoked potentials were recorded from excised adult guinea pig spinal cords before, during, and following exposure to a 0.5-T static magnetic field (SMF). There was no change in response latency during exposure but there was a small, statistically significant, decrease in amplitude. Maximum effect was evident 1 to 2 min after the field was turned on with return to baseline within 1 min after the field was turned off. These results may be explained by a conduction block in the small axon subpopulation due to the effect of static magnetic fields on voltage-activated sodium channels. The relative selectivity of the field is believed to occur because of the relatively greater number of sodium channels present in smaller axons.

Introduction

Moderate intensity static magnetic fields (SMF) have been shown to influence a variety of biological systems, particularly those whose function is closely linked to the function of membrane ion channels. Changes have been demonstrated in the somatosensory-evoked potential in rats [1], in spontaneous central nervous system neuronal activity in cats [2], in neurotransmitter release at the neuromuscular junction in mice [3], and in neuronal action potentials in dissociated cultures of dorsal root ganglia neurons in mice [4]. In all of these studies, it appears that SMFs exert their influence primarily at the synapse and it has been proposed [5] that these fields alter the function of membrane ion channels. The present study was carried out to determine if a moderate intensity static magnetic field is sufficient to influence nonsynaptic axonal excitability in mammalian spinal cord.

Section snippets

Methods

With the approval of the institutional animal utilization committee, studies were carried out on adult female guinea pigs. The spinal cord was removed following anesthetization with ketamine hydrochloride (60 mg/kg), acepromazine maleate (0.6 mg/kg), and xylazine (10 mg/kg). Following removal, a 35–38-mm segment of cord was bathed in oxygenated Krebs solution (in mM: 124 NaCl, 2 KCl, 1.2 KH₂PO₄, 1.3 MgSO₄, 1.2 CaCl₂, 10 dextrose, 26 NaHCO₃, and 10 Na-ascorbate) for 1 h before use. Recordings of

Results

Data were collected from the spinal cords of 10 animals, in 5 of which stability was sufficient to allow detailed analysis. A typical compound action potential is shown in Fig. 1. The mean latency for all control responses was 0.28 ms with a standard deviation of 0.022. There were no changes in latencies during exposure to the magnetic field. The amplitude of the responses varied from 400 to 600 μV. In each experiment, the mean amplitude during the control period was calculated and the percent

Discussion

A theoretical analysis [8] predicted that magnetic fields of at least 24 T would be required to produce sufficient Lorentz forces to slow axonal conduction. This model, however, did not consider the possibility that lower intensity fields might alter the function of ion channels in excitable membranes. It has been shown that the activation kinetics of both calcium [9] and sodium [10] channels are transiently slowed during exposure to static magnetic fields with intensities of only 125 mT. The

Conclusion

The results of this study are consistent with the previous findings that moderate intensity static magnetic fields affect Na⁺ channels. The potential use of these fields for selective small fiber block in both the central and peripheral nervous system needs to be explored further.

Acknowledgements

The authors wish to express their appreciation for the skilled technical assistance of Phyllis Zickmund.

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If this is the case, then the question is how tsSMS affects spinal cord excitability. Previous studies utilizing animal and cellular models have proposed that static magnetic fields can alter membrane ion channel function (Rosen, 2003a; b; Coots et al., 2004). It is therefore possible that in the present study, ion channel function in the motor neuron membranes may have been modulated, resulting in depression of the MEPs.
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Compared with baseline MEP amplitudes were decreased during tsSMS, but not during sham stimulation. Additionally, during the intervention, MEP amplitudes were lower with tsSMS than sham stimulation, although these effects did not last after the intervention ceased.
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Effect of a 0.5-T static magnetic field on conduction in guinea pig spinal cord

Abstract

Introduction

Section snippets

Methods

Results

Discussion

Conclusion

Acknowledgements

Exp. Neurol.

Biochim. Biophys. Acta

J. Neurol. Sci.

J. Neurol. Sci.

Changes in brain evoked potentials under the influence of a permanent magnetic field

Bull. Exp. Biol. Med.

Magnetic field influence on acetylcholine release at the neuromuscular junction

Am. J. Physiol. Cell Physiol. 31

Blockade of sensory neuron action potentials by a static magnetic field in the 10 mT range

Bioelectromagnetics