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Neuron-astrocyte interactions in the medial nucleus of the trapezoid body

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Item Type:Article
Title:Neuron-astrocyte interactions in the medial nucleus of the trapezoid body
Creators Name:Reyes-Haro, D., Mueller, J., Boresch, M., Pivneva, T., Benedetti, B., Scheller, A., Nolte, C. and Kettenmann, H.
Abstract:The calyx of Held (CoH) synapse serves as a model system to analyze basic mechanisms of synaptic transmission. Astrocyte processes are part of the synaptic structure and contact both pre- and postsynaptic membranes. In the medial nucleus of the trapezoid body (MNTB), midline stimulation evoked a current response that was not mediated by glutamate receptors or glutamate uptake, despite the fact that astrocytes express functional receptors and transporters. However, astrocytes showed spontaneous Ca(2+) responses and neuronal slow inward currents (nSICs) were recorded in the postsynaptic principal neurons (PPNs) of the MNTB. These currents were correlated with astrocytic Ca(2+) activity because dialysis of astrocytes with BAPTA abolished nSICs. Moreover, the frequency of these currents was increased when Ca(2+) responses in astrocytes were elicited. NMDA antagonists selectively blocked nSICs while D-serine degradation significantly reduced NMDA-mediated currents. In contrast to previous studies in the hippocampus, these NMDA-mediated currents were rarely synchronized.
Keywords:Amino Acid Transport System X-AG, Anthozoa, Astrocytes, Brain Stem, Calcium, Cell Communication, Chelating Agents, Electric Stimulation, Excitatory Amino Acid Antagonists, Glutamic Acid, Green Fluorescent Proteins, Membrane Potentials, N-Methylaspartate, Nerve Tissue Proteins, Neurons, Glutamate Receptors, N-Methyl-D-Aspartate Receptors, Recombinant Fusion Proteins, Serine, Synapses, Synaptic Transmission, Time Factors, Animals, Mice
Source:Journal of General Physiology
ISSN:0022-1295
Publisher:Rockefeller University Press
Volume:135
Number:6
Page Range:583-594
Date:June 2010
Official Publication:https://doi.org/10.1085/jgp.200910354
PubMed:View item in PubMed

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