Hirrlinger, Johannes

[["dc.bibliographiccitation.firstpage","S23"],["dc.bibliographiccitation.journal","NEURON GLIA BIOLOGY"],["dc.bibliographiccitation.lastpage","S24"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Kaiser, M."],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neusch, C."],["dc.date.accessioned","2018-11-07T11:07:10Z"],["dc.date.available","2018-11-07T11:07:10Z"],["dc.date.issued","2007"],["dc.identifier.isi","000251708800070"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52492"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.publisher.place","New york"],["dc.relation.issn","1740-925X"],["dc.title","Co-enrichment of Kir4.1 and AQP4 channels in spinal cord astrocytes suggests coupling of K+ flux and water transport: swelling experiments using transgenic mouse technology and time lapse 2-photon laser microscopy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","NEURON GLIA BIOLOGY"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2018-11-07T11:07:11Z"],["dc.date.available","2018-11-07T11:07:11Z"],["dc.date.issued","2007"],["dc.format.extent","S109"],["dc.identifier.isi","000251708800336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52494"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.publisher.place","New york"],["dc.relation.issn","1741-0533"],["dc.relation.issn","1740-925X"],["dc.title","Pharmacological inhibition of the NO-pathway blocks microglia migration following a laser lesion in the mouse spinal cord in vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1133"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1144"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Scheller, Anja"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2018-11-07T08:41:42Z"],["dc.date.available","2018-11-07T08:41:42Z"],["dc.date.issued","2010"],["dc.description.abstract","To understand the pathomechanisms of spinal cord injuries will be a prerequisite to develop efficient therapies. By investigating acute lesions of spinal cord white matter in anesthetized mice with fluorescently labeled microglia and axons using in vivo two-photon laser-scanning microscopy (2P-LSM), we identified the messenger nitric oxide (NO) as a modulator of injury-activated microglia. Local tissue damages evoked by high-power laser pulses provoked an immediate attraction of microglial processes. Spinal superfusion with NO synthase and guanylate cyclase inhibitors blocked these extensions. Furthermore, local injection of the NO-donor spermine NONOate (SPNO) or the NO-dependent second messenger cGMP induced efficient migration of microglial cells toward the injection site. High-tissue levels of NO, achieved by uniform superfusion with SPNO and mimicking extended tissue damage, resulted in a fast conversion of the microglial shape from ramified to ameboid indicating cellular activation. When the spinal white matter was preconditioned by increased, ambient ATP (known as a microglial chemoattractant) levels, the attraction of microglial processes to local NO release was augmented, whereas it was abolished at low levels of tissue ATP. Because both signaling molecules, NO and ATP, mediate acute microglial reactions, coordinated pharmacological targeting of NO and purinergic pathways will be an effective mean to influence the innate immune processes after spinal cord injury. (C) 2010 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.20993"],["dc.identifier.isi","000278198400011"],["dc.identifier.pmid","20468054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19527"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","NO Mediates Microglial Response to Acute Spinal Cord Injury Under ATP Control In Vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","NEURON GLIA BIOLOGY"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2018-11-07T11:07:13Z"],["dc.date.available","2018-11-07T11:07:13Z"],["dc.date.issued","2007"],["dc.format.extent","S154"],["dc.identifier.isi","000251708800474"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52503"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.publisher.place","New york"],["dc.relation.issn","1740-925X"],["dc.title","In vivo observations of axon-microglia interactions in the mouse spinal cord"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","119"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","132"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Saab, Aiman S."],["dc.contributor.author","Tzvetavona, Iva D."],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Baltan, Selva"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Jahn, Hannah M."],["dc.contributor.author","Huang, Wenhui"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Pérez-Samartín, Alberto"],["dc.contributor.author","Pérez-Cerdá, Fernando"],["dc.contributor.author","Bakhtiari, Davood"],["dc.contributor.author","Matute, Carlos"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2017-09-07T11:44:48Z"],["dc.date.available","2017-09-07T11:44:48Z"],["dc.date.issued","2016"],["dc.description.abstract","Oligodendrocytes make myelin and support axons metabolically with lactate. However, it is unknown how glucose utilization and glycolysis are adapted to the different axonal energy demands. Spiking axons release glutamate and oligodendrocytes express NMDA receptors of unknown function. Here we show that the stimulation of oligodendroglial NMDA receptors mobilizes glucose transporter GLUT1, leading to its incorporation into the myelin compartment in vivo. When myelinated optic nerves from conditional NMDA receptor mutants are challenged with transient oxygen-glucose deprivation, they show a reduced functional recovery when returned to oxygen-glucose but are indistinguishable from wild-type when provided with oxygen-lactate. Moreover, the functional integrity of isolated optic nerves, which are electrically silent, is extended by preincubation with NMDA, mimicking axonal activity, and shortened by NMDA receptor blockers. This reveals a novel aspect of neuronal energy metabolismin which activity-dependent glutamate release enhances oligodendroglial glucose uptake and glycolytic support of fast spiking axons."],["dc.identifier.doi","10.1016/j.neuron.2016.05.016"],["dc.identifier.gro","3141651"],["dc.identifier.isi","000382394300016"],["dc.identifier.pmid","27292539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5454"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1097-4199"],["dc.relation.issn","0896-6273"],["dc.title","Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2620"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","2628"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Kaiser, Melanie"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2018-11-07T10:48:52Z"],["dc.date.available","2018-11-07T10:48:52Z"],["dc.date.issued","2007"],["dc.description.abstract","In glial cells, inwardly rectifying K+ channels (Kir) control extracellular [K+](o) homeostasis by uptake of K+ from the extracellular space and release of K+ into the microvasculature. Kir channels were also recently implicated in K+-associated water influx and cell swelling. We studied the time-dependent expression and functional implication of the glial Kir4.1 channel for astroglial swelling in a spinal cord edema model. In this CNS region, Kir4.1 is expressed on astrocytes from the second postnatal week on and co-localizes with aquaporin 4 (AQP4). Swelling of individual astrocytes in response to osmotic stress and to pharmacological Kir blockade were analyzed by time-lapse-two-photon laser-scanning microscopy in situ. Application of 30% hypotonic solution induced astroglial soma swelling whereas no swelling was observed on astroglial processes or endfeet. Co-application of hypotonic solution and Ba2+, a Kir channel blocker, induced prominent swelling of astroglial processes. In Kir4.1(-/-) mice, however, somatic as well as process swelling was observed upon application of 30% hypotonic solutions. No additional effect was provoked upon co-application with Ba2+. Our experiments show that Kir channels prevent glial process swelling under osmotic stress. The underlying Kir channel subunit that controls glial process swelling is Kir4.1, whereas changes of the glial soma are not substantially related to Kir4.1."],["dc.identifier.doi","10.1111/j.1471-4159.2007.04979.x"],["dc.identifier.isi","000207062600008"],["dc.identifier.pmid","17953658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48301"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3042"],["dc.title","Kir4.1 channels regulate swelling of astroglial processes in experimental spinal cord edema"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]