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Cited by 1,003

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Direct Signaling from Astrocytes to Neurons in Cultures of Mammalian Brain Cells

Nedergaard, Maiken·1994·Science

Abstract

Although astrocytes have been considered to be supportive, rather than transmissive, in the adult nervous system, recent studies have challenged this assumption by demonstrating that astrocytes possess functional neurotransmitter receptors. Astrocytes are now shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons. When a focal electric field potential was applied to single astrocytes in mixed cultures of rat forebrain astrocytes and neurons, a prompt elevation of calcium occurred in the target cell. This in turn triggered a wave of calcium increase, which propagated from astrocyte to astrocyte. Neurons resting on these astrocytes responded with large increases in their concentration of cytosolic calcium. The gap junction blocker octanol attenuated the neuronal response, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically. This neuronal response to local astrocytic stimulation may mediate local intercellular communication within the brain.

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Metadata

Authors
Nedergaard, M.
Venue
Science
Published
1994-03-25
Volume
263
Issue
5154
Pages
1768-1771
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2065843356
Cited by
1,003
References
1
FWCI
21.20
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Direct Signaling from Astrocytes to Neurons in Cultures of Mammalian Brain Cells. https://app.cochat.ai/papers/10.1126/science.8134839
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Nedergaard, M. (1994). Direct Signaling from Astrocytes to Neurons in Cultures of Mammalian Brain Cells. Science. https://doi.org/10.1126/science.8134839

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.