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Cited by 14Neuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration MechanismsPain Mechanisms and Treatments

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Glial-toxin-mediated disruption of spinal cord locomotor network function and its modulation by 5-HT

Baudoux, S., Parker, D.·2008·Neuroscience
DOI 10.1016/j.neuroscience.2008.03.034
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Abstract

While it is established that glial cells actively influence neuronal and synaptic properties, the functional effects of glial-neuronal interactions are still not well understood. To address the role of glia at the network level we have examined the effects of the specific gliotoxin L-aminoadipic acid on the locomotor network output and cellular and synaptic properties in the lamprey spinal cord. The gliotoxic effect of aminoadipic acid was associated with a specific depolarization of glial cells. Aminoadipic acid depolarized the membrane potential of spinal cord neurons, suggesting a functional link between glia and neurons. The depolarization was significantly reduced by glutamate receptor antagonists in adults, but by gap junction blockers in larvae, suggesting a developmental difference in glial-neuronal interactions. Aminoadipic acid also reduced the amplitude of monosynaptic excitatory postsynaptic potentials (EPSPs), an effect that was not associated with changes in the presynaptic release probability or postsynaptic response to glutamate. These cellular and synaptic effects of aminoadipic acid were associated with disruption of the locomotor network output. This could not be accounted for by changes in glutamate uptake or potassium buffering by glia, suggesting a direct role for glia in the network. Interestingly, we found that the aminoadipic acid-evoked disruption of network activity and reduction of monosynaptic EPSP amplitudes did not occur in the presence of the e…

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Metadata

Authors
Baudoux, S., & Parker, D.
Affiliations
University of Cambridge (GB)
Corresponding author
Parker, D.
ORCID
Parker, D.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2008-06
Volume
153
Issue
4
Pages
1332-1343
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2008.03.034
OpenAlex
W2001389948
Cited by
14
References
0
Citations by year
2022: 1 · 2021: 1 · 2019: 1 · 2017: 1 · 2015: 1 · 2014: 3
FWCI
0.87
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
Wellcome Trust
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
Keywords
neuron-glia interactions, gliotoxin, lamprey, serotonin, monosynaptic excitatory postsynaptic potentials, glial depolarization, gap junctions, glutamate receptor antagonists, developmental differences, glutamate uptake, potassium buffering, network activity
MeSH terms
Anesthetics, Local, Animals, Drug Interactions, Female, Lampreys, Male, Nerve Net, Neuroglia, Serotonin, Spinal Cord, Tetrodotoxin, Time Factors, 2-Aminoadipic Acid, N-Methylaspartate, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, In Vitro Techniques

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