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Neuroscience. 2014 Jan 31;258:184-91. doi: 10.1016/j.neuroscience.2013.11.009. Epub 2013 Nov 14.

Sensory transduction of weak electromagnetic fields: role of glutamate neurotransmission mediated by NMDA receptors.

Author information

1
School of Allied Health Professions, LSU Health Sciences Center, P.O. Box 33932, Shreveport, LA 71130-3932, USA.
2
Natural Sciences Department, Daemen College, 4380 Main Street, Amherst, NY 14226, USA.
3
Department of Neurology, LSU Health Sciences Center, P.O. Box 33932, Shreveport, LA 71130-3932, USA. Electronic address: amarino@lsuhsc.edu.

Abstract

Subliminal electromagnetic fields (EMFs) triggered nonlinear evoked potentials in awake but not anesthetized animals, and increased glucose metabolism in the hindbrain. Field detection occurred somewhere in the head and possibly was an unrecognized function of sensory neurons in facial skin, which synapse in the trigeminal nucleus and project to the thalamus via glutamate-dependent pathways. If so, anesthetic agents that antagonize glutamate neurotransmission would be expected to degrade EMF-evoked potentials (EEPs) to a greater extent than agents having different pharmacological effects. We tested the hypothesis using ketamine which blocks N-methyl-d-aspartate (NMDA) receptors (NMDARs), and xylazine which is an α₂-adrenoreceptor agonist. Electroencephalograms (EEGs) of rats were examined using recurrence analysis to observe EEPs in the presence and absence of ketamine and/or xylazine anesthesia. Auditory evoked potentials (AEPs) served as positive controls. The frequency of observation of evoked potentials in a given condition (wake or anesthesia) was compared with that due to chance using the Fisher's exact test. EEPs were observed in awake rats but not while they were under anesthesia produced using a cocktail of xylazine and ketamine. In another experiment each rat was measured while awake and while under anesthesia produced using either xylazine or ketamine. EEPs and AEPs were detected during wake and under xylazine (P<0.05 in each of the four measurements). In contrast, neither EEPs nor AEPs were observed when anesthesia was produced partly or wholly using ketamine. The duration and latency of the EEPs was unaltered by xylazine anesthesia. The afferent signal triggered by the transduction of weak EMFs was likely mediated by NMDAR-mediated glutamate neurotransmission.

KEYWORDS:

%D; %R; ABR; AEPs; Coiflet; Daubechies; Db; EEGs; EEPs; EMF-evoked potentials; EMFs; N-methyl-d-aspartate; NMDA; NMDA receptor; NMDAR; XK; amplitude threshold coefficients; analysis of brain recurrence; atc; auditory evoked potentials; cerebellum; coif; electroencephalograms; electromagnetic fields; evoked potentials; ketamine; nonlinear analysis; percent determinism; percent recurrence; xylazine; xylazine and ketamine

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