title: Blockade of sensory neuron action potentials by a static magnetic field in the 10 mT range.
abstract: To characterize the inhibitory effect of a static magnetic field, action potentials (AP) were elicited by intracellular application of 1 ms depolarizing current pulses of constant amplitude to the somata of adult mouse dorsal root ganglion neurons in monolayer dissociated cell culture. During the control period, < 5% of stimuli failed to elicit AP. During exposure to an approximately 11 mT static magnetic field at the cell position produced by an array of four permanent center-charged neodymium magnets of alternating polarity (MAG-4A), 66% of stimuli failed to elicit AP. The number of failures was maximal after about 200-250 s in the field and returned gradually to baseline over 400-600 s. A direct or indirect effect on the conformation of AP generating sodium channels could account for these results because 1) failure was preceded often by reduction of maximal rate of rise, an indirect measure of sodium current; 2) recovery was significantly prolonged in more than one-half of neurons that were not stimulated during exposure to the MAG-4A field; and 3) resting membrane potential, input resistance, and chronaxie were unaffected by the field. The effect was diminished or prevented by moving the MAG-4A array along the X or Z axis away from the neuron under study and by increasing the distance between magnets in the XY plane. Reduction of AP firing during exposure to the approximately 0.1 mT field produced by a MAG-4A array of micromagnets was about the same as that produced by a MAG-4A array of the large magnets above. The approximately 28 mT field produced at cell position by two magnets of alternating polarity and the approximately 88 mT field produced by a single magnet had no significant effect on AP firing. These findings suggest that field strength alone cannot account for AP blockade.
authors.affiliation: Department of Neurology, Department of Veterans Affairs Medical Center, Nashville, Tennessee, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: McLean
authors.forename: R R
authors.initials: RR
authors.lastname: Holcomb
authors.forename: A W
authors.initials: AW
authors.lastname: Wamil
authors.forename: J D
authors.initials: JD
authors.lastname: Pickett
authors.forename: A V
authors.initials: AV
authors.lastname: Cavopol
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D002478:Cells, Cultured; D018118:Chloride Channels / Q000502:physiology; D002907:Chronaxy / Q000502:physiology; D017097:Electric Impedance; D004558:Electric Stimulation; D005727:Ganglia, Spinal / Q000502:physiology; D008280:Magnetics / Q000009:adverse effects*; D008564:Membrane Potentials / Q000502:physiology; D051379:Mice; D009354:Neodymium; D009412:Nerve Fibers / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000502:physiology; D009431:Neural Conduction; D009433:Neural Inhibition; D009475:Neurons, Afferent / Q000502:physiology*; D015222:Sodium Channels / Q000502:physiology
chemical_list: D018118:Chloride Channels; D015222:Sodium Channels; D009354:Neodymium