Cited by 158Neuroscience and Neuropharmacology ResearchAmino Acid Enzymes and MetabolismNeuroinflammation and Neurodegeneration Mechanisms

Glutamate‐mediated neuronal–glial transmission

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Verkhratsky, Alexei, Kirchhoff, Frank·2007·Journal of Anatomy

Abstract

The brain is the most complex organ of the human body. It is composed of several highly specialized and heterogeneous populations of cells, represented by neurones (e.g. motoneurons, projection neurons or interneurons), and glia represented by astrocytes, oligodendrocytes and microglia. In recent years there have been numerous studies demonstrating close bidirectional communication of neurons and glia at structural and functional levels. In particular, the excitatory transmitter glutamate has been shown to evoke a variety of responses in astrocytes and oligodendrocytes in the healthy as well as the diseased brain. Here we overview the multitude of glutamate sensing molecules expressed in glia and describe some general experiments which have been performed to identify the glutamate‐responsive molecules, i.e. the ionotropic and metabotropic glutamate receptors as well as the glutamate transporters. We also discuss a transgenic mouse model that permits detailed and specific investigations of the role of glial glutamate receptors.

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Crossref · 10.1111/j.1469-7580.2007.00734.x

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  • Delivery of energy substrates can be adjusted on demand through modulation of neurovascular coupling or via neuronal signaling to astrocytes.

    “This process can be adjusted on demand either through modulation of neurovascular coupling15–17 or via neuronal signaling to astrocytes18.”

    From Energy paradox in REM sleep: balancing supply and consumption in brain metabolism (2026) · cites this paper as [17]

    The Conclusions (page unavailable) state that synaptic glutamate release triggers signaling responses in glial cells, supporting the cited neuronal-signaling-to-astrocytes pathway. The introductory passage (labeled Abstract; page unavailable) also mentions glial energy support, but our copy does not establish that this signaling adjusts energy-substrate delivery on demand. The neurovascular-coupling alternative is attributed to citations 15–17, not this source. (LLM, conf=0.78)

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Research works printed but not linked: 3

  1. Exner S, 1894, Entwurf zur physiologischen Erklärung der Psychischen Erscheinungen
  2. 10.1242/jeb.02208 · DOI
  3. Swanson RA, 2005, Neuroglia, 346

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Authors
Verkhratsky, A., & Kirchhoff, F.
Affiliations
  • University of Manchester (GB)
  • Max Planck Society (DE)
Venue
Journal of Anatomy
Publisher
Wiley
Published
2007-05-15
Volume
210
Issue
6
Pages
651-660
ISSN
  • 0021-8782 (ISSN-L)
  • 1469-7580
OpenAlex
W2050984501
Cited by
156
References
103
Citations by year
2026: 3 · 2025: 2 · 2024: 1 · 2023: 5 · 2022: 10 · 2021: 10 · 2020: 8 · 2019: 8 · 2018: 5 · 2017: 9 · 2016: 7 · 2015: 10 · 2014: 5 · 2013: 12 · 2012: 11
FWCI
1.01
Type
journal article
Language
en
Open access
Locations
  • Journal of Anatomy (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
  • MPG.PuRe (Max Planck Society) (submittedVersion)
Funders
  • Wellcome Trust
  • Deutsche Forschungsgemeinschaft
  • National Institutes of Health
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
glutamate, astrocytes, oligodendrocytes, microglia, ionotropic glutamate receptors, metabotropic glutamate receptors, glutamate transporters, transgenic mouse model
MeSH terms
Animals, Brain, Glutamates, Humans, Mice, Transgenic, Neuroglia, Neurons, Receptors, Glutamate, Models, Animal, Amino Acid Transport System X-AG, Mice

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