Cited by 369Vagus Nerve Stimulation ResearchEpilepsy research and treatmentNeurological disorders and treatments

Effects of Vagal Stimulation on Experimentally Induced Seizures in Rats

Woodbury, Dixon M., Woodbury, J. Walter·1990·Epilepsia

Abstract

Summary: Repetitive stimulation of the vagus nerve inhibits chemically induced seizures in dogs. We report here the results and conclusions from studies designed to answer some of the immediate questions raised by this finding. (1) Maximal stimulation of vagal C fibers at frequencies greater than 4 Hz prevents or reduces chemically and electrically induced seizures in young male rats. (2) Antiepileptic potency is directly related to the fraction of vagal C fibers stimulated. (3) Vagal stimulation shortens but does not shut down a chemical seizure once it has begun. (4) In rats, optimal stimulus frequency is approximately 10–20 Hz; duration of stimulus, 0.5‐1 ms; and stimulus strength, 0.2‐0.5 mA/mm 2 of nerve cross‐section. These results, when taken together with similar results obtained from dogs, monkeys, and humans, strongly suggest that periodic stimulation of the vagus nerve using appropriate stimulation parameters is a powerful method for preventing seizures. The data from the literature suggest that the antiepileptic actions of vagal stimulation are largely mediated by widespread release of GAB A and glycine in the brainstem and cerebral cortex. The probable pathway is via projections from the nucleus of the solitary tract to the reticular formation and thence by diffuse projections to the cortex and other areas. Intermittent vagal stimulation has the potentiality of reducing the number and/or the intensity of seizures in patients with intractable epilepsy. These results indicate that feasibility studies in humans should be continued and expanded.

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Crossref · 10.1111/j.1528-1157.1990.tb05852.x

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  • Peripheral activation of vagal lung afferents, in theory, activates central parasympathetic representations and deactivates sympathetic-related regions and neurotransmitter systems at higher levels.

    “such activation will, in theory, activate central parasympathetic representations and deactivate sympathetic-related regions and neurotransmitter systems at higher levels”

    From Fear and the Defense Cascade (2015) · cites this paper as [150]

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Authors
Woodbury, D. M., & Woodbury, J. W.
Affiliations
University of Utah (US)
Corresponding author
Woodbury, Dixon M.
Venue
Epilepsia
Publisher
Wiley
Published
1990-06
Volume
31
Issue
s2
Pages
S7-19
ISSN
  • 0013-9580 (ISSN-L)
  • 1528-1167
OpenAlex
W2059355906
Cited by
369
References
0
Citations by year
2026: 2 · 2025: 11 · 2024: 13 · 2023: 11 · 2022: 15 · 2021: 10 · 2020: 15 · 2019: 12 · 2018: 15 · 2017: 10 · 2016: 13 · 2015: 22 · 2014: 10 · 2013: 13 · 2012: 15
FWCI
4.81
Type
journal article
Language
en
Open access
closed
Locations
  • Epilepsia (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5k06ns013838-29)
  • National Institute of Neurological Disorders and Stroke (5 KO6-NS-13838)
Topics
  • Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
  • Health Sciences › Medicine › Neurology › Neurological disorders and treatments
Keywords
vagus nerve stimulation, seizure prevention, antiepileptic effect, stimulation frequency, seizure induction, GABA release, glycine release, nucleus tractus solitarius, reticular formation, drug-resistant epilepsy
MeSH terms
Action Potentials, Animals, Electric Stimulation, Electric Stimulation Therapy, Heart Rate, Male, Neural Conduction, Neural Pathways, Pentylenetetrazole, Respiration, Seizures, Vagus Nerve, 3-Mercaptopropionic Acid, Rats

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