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Letters to Nature
Nature 369, 744 - 747 (30 June 1994); doi:10.1038/369744a0

Glutamate-mediated astrocyte–neuron signalling

Vladimir Parpura*, Trent A. Basarsky*, Fang Liu, Ksenija Jeftinija, Srdija Jeftinija & Philip G. Haydon*§

*Department of Zoology and Genetics, Neuroscience Program, or Department of Veterinary Anatomy, Iowa State University, 339 Science II, Ames, Iowa 50011, USA
§ To whom correspondence should be addressed

NEUROTRANSMITTER released from neurons is known to signal to neighbouring neurons and glia1–3 Here we demonstrate an additional signalling pathway in which glutamate is released from astrocytes and causes an NMDA (N-methyl-d-aspartate) receptor-mediated increase in neuronal calcium. Internal calcium was elevated and glutamate release stimulated by application of the neuro-ligand bradykinin to cultured astrocytes. Elevation of astrocyte internal calcium was also sufficient to induce glutamate release. To determine whether this released glutamate signals to neurons, we studied astrocyte–neuron co-cultures. Bradykinin significantly increased calcium levels in neurons co-cultured with astrocytes, but not in solitary neurons. The glutamate receptor antagonists d-2-amino-5-phosphonopentanoic acid and d-glutamylglycine prevented bradykinin-induced neuronal calcium elevation. When single astrocytes were directly stimulated to increase internal calcium and release glutamate, calcium levels of adjacent neurons were increased; this increase could be blocked by d-glutamylglycine. Thus, astrocytes regulate neuronal calcium levels through the calcium-dependent release of glutamate.

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