title: Neuron-astrocyte interactions in the medial nucleus of the trapezoid body.
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.
authors.affiliation: Cellular Neuroscience, Max Delbrück Center for Molecular Medicine, 13092 Berlin, Germany.
authors.forename: Daniel
authors.initials: D
authors.lastname: Reyes-Haro
authors.forename: Jochen
authors.initials: J
authors.lastname: Müller
authors.forename: Margarethe
authors.initials: M
authors.lastname: Boresch
authors.forename: Tatjyana
authors.initials: T
authors.lastname: Pivneva
authors.forename: Bruno
authors.initials: B
authors.lastname: Benedetti
authors.forename: Anja
authors.initials: A
authors.lastname: Scheller
authors.forename: Christiane
authors.initials: C
authors.lastname: Nolte
authors.forename: Helmut
authors.initials: H
authors.lastname: Kettenmann
mesh_terms: D027322:Amino Acid Transport System X-AG / Q000378:metabolism; D000818:Animals; D037421:Anthozoa / Q000235:genetics; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D001933:Brain Stem / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002450:Cell Communication / Q000187:drug effects; D002614:Chelating Agents / Q000494:pharmacology; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005904:Glial Fibrillary Acidic Protein; D018698:Glutamic Acid / Q000378:metabolism; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D008564:Membrane Potentials; D051379:Mice; D008822:Mice, Transgenic; D016202:N-Methylaspartate / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D017470:Receptors, Glutamate / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D012694:Serine / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects; D013997:Time Factors
chemical_list: D027322:Amino Acid Transport System X-AG; D002614:Chelating Agents; D018691:Excitatory Amino Acid Antagonists; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D011993:Recombinant Fusion Proteins; C485184:enhanced green fluorescent protein; C528900:glial fibrillary astrocytic protein, mouse; D049452:Green Fluorescent Proteins; D018698:Glutamic Acid; D012694:Serine; D016202:N-Methylaspartate; D002118:Calcium