Glutamate Released from Glial Cells Synchronizes Neuronal Activity in the Hippocampus

• Published in: The Journal of neuroscience 2004-08, Vol.24 (31), p.6920-6927
• Main Authors: Angulo, Maria Cecilia, Kozlov, Andrei S, Charpak, Serge, Audinat, Etienne
• Format: Article
• Language: English
• Subjects: Amino Acid Transport System X-AG; Animals; Astrocytes - physiology; Cellular/Molecular; Glutamic Acid - physiology; Hippocampus - physiology; Humans; In Vitro Techniques; Life Sciences; Neuroglia - physiology; Neurons and Cognition; Pyramidal Cells - physiology; Rats; Receptors, N-Methyl-D-Aspartate; Synaptic Transmission - physiology
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/JNEUROSCI.0473-04.2004

Glial cells of the nervous system directly influence neuronal and synaptic activities by releasing transmitters. However, the physiological consequences of this glial transmitter release on brain information processing remain poorly understood. We demonstrate here in hippocampal slices of 2- to 5-week-old rats that glutamate released from glial cells generates slow transient currents (STCs) mediated by the activation of NMDA receptors in pyramidal cells. STCs persist in the absence of neuronal and synaptic activity, indicating a nonsynaptic origin of the source of glutamate. Indeed, STCs occur spontaneously but can also be induced by pharmacological tools known to activate astrocytes and by the selective mechanical stimulation of single nearby glial cells. Bath application of the inhibitor of the glutamate uptake dl-threo-beta-benzyloxyaspartate increases both the frequency of STCs and the amplitude of a tonic conductance mediated by NMDA receptors and probably also originated from glial glutamate release. By using dual recordings, we observed synchronized STCs in pyramidal cells having their soma distant by