Now showing 1 - 2 of 2
  • 2013Journal Article
    [["dc.bibliographiccitation.artnumber","e1001604"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Fruehbeis, Carsten"],["dc.contributor.author","Froehlich, Dominik"],["dc.contributor.author","Kuo, Wen Ping"],["dc.contributor.author","Amphornrat, Jesa"],["dc.contributor.author","Thilemann, Sebastian"],["dc.contributor.author","Saab, Aiman S."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Klugmann, Matthias"],["dc.contributor.author","Trotter, Jacqueline"],["dc.contributor.author","Kraemer-Albers, Eva-Maria"],["dc.date.accessioned","2018-11-07T09:22:56Z"],["dc.date.available","2018-11-07T09:22:56Z"],["dc.date.issued","2013"],["dc.description.abstract","Reciprocal interactions between neurons and oligodendrocytes are not only crucial for myelination, but also for long-term survival of axons. Degeneration of axons occurs in several human myelin diseases, however the molecular mechanisms of axon-glia communication maintaining axon integrity are poorly understood. Here, we describe the signal-mediated transfer of exosomes from oligodendrocytes to neurons. These endosome-derived vesicles are secreted by oligodendrocytes and carry specific protein and RNA cargo. We show that activity-dependent release of the neurotransmitter glutamate triggers oligodendroglial exosome secretion mediated by Ca2+ entry through oligodendroglial NMDA and AMPA receptors. In turn, neurons internalize the released exosomes by endocytosis. Injection of oligodendroglia-derived exosomes into the mouse brain results in functional retrieval of exosome cargo in neurons. Supply of cultured neurons with oligodendroglial exosomes improves neuronal viability under conditions of cell stress. These findings indicate that oligodendroglial exosomes participate in a novel mode of bidirectional neuron-glia communication contributing to neuronal integrity."],["dc.identifier.doi","10.1371/journal.pbio.1001604"],["dc.identifier.isi","000322592700008"],["dc.identifier.pmid","23874151"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9144"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29458"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Neurotransmitter-Triggered Transfer of Exosomes Mediates Oligodendrocyte-Neuron Communication"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
    Details DOI PMID PMC WOS
  • 2017Journal Article
    [["dc.bibliographiccitation.artnumber","e24241"],["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Saab, Aiman S."],["dc.contributor.author","Winkler, Ulrike"],["dc.contributor.author","Marx, Grit"],["dc.contributor.author","Imamura, Hiromi"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.date.accessioned","2017-05-22T13:48:50Z"],["dc.date.accessioned","2021-10-27T13:21:00Z"],["dc.date.available","2017-05-22T13:48:50Z"],["dc.date.available","2021-10-27T13:21:00Z"],["dc.date.issued","2017"],["dc.description.abstract","In several neurodegenerative diseases and myelin disorders, the degeneration profiles of myelinated axons are compatible with underlying energy deficits. However, it is presently impossible to measure selectively axonal ATP levels in the electrically active nervous system. We combined transgenic expression of an ATP-sensor in neurons of mice with confocal FRET imaging and electrophysiological recordings of acutely isolated optic nerves. This allowed us to monitor dynamic changes and activity-dependent axonal ATP homeostasis at the cellular level and in real time. We find that changes in ATP levels correlate well with compound action potentials. However, this correlation is disrupted when metabolism of lactate is inhibited, suggesting that axonal glycolysis products are not sufficient to maintain mitochondrial energy metabolism of electrically active axons. The combined monitoring of cellular ATP and electrical activity is a novel tool to study neuronal and glial energy metabolism in normal physiology and in models of neurodegenerative disorders."],["dc.identifier.doi","10.7554/eLife.24241"],["dc.identifier.pmid","28414271"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14464"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91987"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2050-084X"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Monitoring ATP dynamics in electrically active white matter tracts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
    Details DOI PMID PMC