Sensory Transduction of Weak Electromagnetic Fields: Role of Glutamate Neurotransmission Mediated by NMDA Receptors.

Author: Frilot C 2nd, Carrubba S, Marino AA.
Affiliation: School of Allied Health Professions, LSU Health Sciences Center, P.O. Box 33932, Shreveport, LA 71130-3932, USA.
Conference/Journal: Neuroscience.
Date published: 2013 Nov 14
Other: Pages: S0306-4522(13)00949-4 , Special Notes: doi: 10.1016/j.neuroscience.2013.11.009 , Word Count: 272



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 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 Fisher's exact test. EEPs were observed in awake rats but not while they under anesthesia produced using a cocktail of ketamine and xylazine. In another experiment each rat was measured while awake and while under anesthesia produced using either ketamine or xylazine. 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 transduction of weak EMFs was likely mediated by NMDAR-mediated glutamate neurotransmission.
Copyright © 2013. Published by Elsevier Ltd.
KEYWORDS:
Cerebellum, Electromagnetic fields, Evoked potentials, Ketamine, Nonlinear analysis, Xylazine

PMID: 24239718