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

Neuroscience · 2014 · Mixed · Low evidence

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MixedLow evidencePaper 4560

Study snapshot

PublicationNeuroscience · 2014

Study typeanimal

Reported directionMixed

Evidence ratingLow

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.

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Study typeanimal

Effect directionmixed

PopulationRats (awake and under anesthesia with ketamine and/or xylazine)

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

EMF-evoked potentials (EEPs) were observed in awake rats but not under anesthesia with a ketamine+xylazine cocktail. In within-animal comparisons, EEPs and AEPs were detected during wake and under xylazine anesthesia (P<0.05), but neither EEPs nor AEPs were observed when anesthesia involved ketamine. The authors conclude the afferent signal from weak EMF transduction was likely mediated by NMDA receptor–mediated glutamate neurotransmission.

Outcomes measured

Electromagnetic field-evoked potentials (EEPs) in EEG
Auditory evoked potentials (AEPs) in EEG (positive control)
Duration and latency of EEPs

Limitations

EMF exposure parameters (e.g., frequency, intensity, duration) are not reported in the abstract.
Sample size is not stated in the abstract.
Findings are in rats; generalizability to humans is not addressed in the abstract.
Ketamine suppressed both EMF-evoked and auditory evoked potentials, suggesting potential non-specific effects on evoked potential detection under ketamine anesthesia.

View raw extracted JSON

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  "population": "Rats (awake and under anesthesia with ketamine and/or xylazine)",
  "sample_size": null,
  "outcomes": [
    "Electromagnetic field-evoked potentials (EEPs) in EEG",
    "Auditory evoked potentials (AEPs) in EEG (positive control)",
    "Duration and latency of EEPs"
  ],
  "main_findings": "EMF-evoked potentials (EEPs) were observed in awake rats but not under anesthesia with a ketamine+xylazine cocktail. In within-animal comparisons, EEPs and AEPs were detected during wake and under xylazine anesthesia (P<0.05), but neither EEPs nor AEPs were observed when anesthesia involved ketamine. The authors conclude the afferent signal from weak EMF transduction was likely mediated by NMDA receptor–mediated glutamate neurotransmission.",
  "effect_direction": "mixed",
  "limitations": [
    "EMF exposure parameters (e.g., frequency, intensity, duration) are not reported in the abstract.",
    "Sample size is not stated in the abstract.",
    "Findings are in rats; generalizability to humans is not addressed in the abstract.",
    "Ketamine suppressed both EMF-evoked and auditory evoked potentials, suggesting potential non-specific effects on evoked potential detection under ketamine anesthesia."
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic fields",
    "weak EMF",
    "sensory transduction",
    "evoked potentials",
    "EEG",
    "rats",
    "ketamine",
    "xylazine",
    "NMDA receptor",
    "glutamate neurotransmission",
    "trigeminal nucleus",
    "thalamus"
  ],
  "suggested_hubs": [
    {
      "slug": "mechanisms-neurobiology",
      "weight": 0.78,
      "reason": "Animal EEG study proposing NMDA/glutamate-mediated mechanism for detection/transduction of weak EMFs."
    },
    {
      "slug": "occupational-exposure",
      "weight": 0,
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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1016/j.neuroscience.2013.11.009
PubMed: 24239718

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