Hirrlinger, Johannes

[["dc.bibliographiccitation.firstpage","1358"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","1365"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Grass, D."],["dc.contributor.author","Pawlowski, P. G."],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Papadopoulos, Nestoras"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Hulsmann, S."],["dc.date.accessioned","2018-11-07T10:51:10Z"],["dc.date.available","2018-11-07T10:51:10Z"],["dc.date.issued","2004"],["dc.description.abstract","A population of neurons in the caudal medulla generates the rhythmic activity underlying breathing movements. Although this neuronal network has attracted great attention for studying neuronal aspects of synaptic transmission, functions of glial cells supporting this neuronal activity remain unclear. To investigate the role of astrocytes in the respiratory network, we applied electrophysiological and immunohistochemical techniques to characterize astrocytes in regions involved in the generation and transmission of rhythmic activity. In the ventral respiratory group and the hypoglossal nucleus (XII) of acutely isolated brainstem slices, we analyzed fluorescently labeled astrocytes obtained from TgN(GFAP-EGFP) transgenic mice with the whole-cell voltage-clamp technique. Three subpopulations of astrocytes could be discerned by their distinct membrane current profiles. A first group of astrocytes was characterized by nonrectifying, symmetrical and voltage-independent potassium currents and a robust glutamate transporter response to D-aspartate. A second group of astrocytes showed additional A-type potassium currents, whereas a third group, identified by immunolabeling for the glial progenitor marker NG2, expressed outwardly rectifying potassium currents, smaller potassium inward currents, and only minimal D-aspartate-induced transporter currents. Astrocytes of all groups showed kainate-induced inward currents. We conclude that most of the astrocytes serve as a buffer system of excess extracellular glutamate and potassium; however, a distinct cell population (NG2-positive, A-type potassium currents) may play an important role for network plasticity."],["dc.identifier.doi","10.1523/JNEUROSCI.4022-03.2004"],["dc.identifier.isi","000188896100012"],["dc.identifier.pmid","14960607"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Diversity of functional astroglial properties in the respiratory network"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","1843"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurophysiology"],["dc.bibliographiccitation.lastpage","1852"],["dc.bibliographiccitation.volume","95"],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Papadopoulos, Nestoras"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Maletzki, Iris"],["dc.contributor.author","Winter, S M"],["dc.contributor.author","Hirrlinger, J"],["dc.contributor.author","Handschuh, M."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Hülsmann, Swen"],["dc.date.accessioned","2017-09-07T11:53:20Z"],["dc.date.available","2017-09-07T11:53:20Z"],["dc.date.issued","2006"],["dc.description.abstract","Ongoing rhythmic neuronal activity in the ventral respiratory group (VRG) of the brain stem results in periodic changes of extracellular K+. To estimate the involvement of the weakly inwardly rectifying K+ channel Kir4.1 (KCNJ10) in extracellular K+ clearance, we examined its functional expression in astrocytes of the respiratory network. Kir4.1 was expressed in astroglial cells of the VRG, predominantly in fine astrocytic processes surrounding capillaries and in close proximity to VRG neurons. Kir4.1 expression was up-regulated during early postnatal development. The physiological role of astrocytic Kir4.1 was studied using mice with a null mutation in the Kir4.1 channel gene that were interbred with transgenic mice expressing the enhanced green fluorescent protein in their astrocytes. The membrane potential was depolarized in astrocytes of Kir4.1(-/-) mice, and Ba2+-sensitive inward K+ currents were diminished. Brain slices from Kir4.1(-/-) mice, containing the pre-Botzinger complex, which generates a respiratory rhythm, did not show any obvious differences in rhythmic bursting activity compared with wild-type controls, indicating that the lack of Kir4.1 channels alone does not impair respiratory network activity. Extracellular K+ measurements revealed that Kir4.1 channels contribute to extracellular K+ regulation. Kir4.1 channels reduce baseline K+ levels, and they compensate for the K+ undershoot. Our data indicate that Kir4.1 channels 1) are expressed in perineuronal processes of astrocytes, 2) constitute the major part of the astrocytic Kir conductance, and 3) contribute to regulation of extracellular K+ in the respiratory network."],["dc.identifier.doi","10.1152/jn.00996.2005"],["dc.identifier.gro","3143730"],["dc.identifier.isi","000235477900049"],["dc.identifier.pmid","16306174"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1276"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0022-3077"],["dc.title","Lack of the Kir4.1 channel subunit abolishes K+ buffering properties of astrocytes in the ventral respiratory group: Impact on extracellular K+ regulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2235"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","2239"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Hulsmann, S."],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2018-11-07T10:45:08Z"],["dc.date.available","2018-11-07T10:45:08Z"],["dc.date.issued","2004"],["dc.description.abstract","Within the tripartite structure of vertebrate synapses, enwrapping astroglial processes regulate synaptic transmission by transmitter uptake and by direct transmitter release. We applied confocal and two-photon laser scanning microscopy to acutely isolated slices prepared from the brainstem of transgenic TgN(GFAP-EGFP) mice. In transversal sections fluorescently labelled astrocytes are evenly distributed throughout the tissue. Astroglial processes contacted neuronal somata and enwrapped active synaptic terminals as visualized using FM1-43 staining in situ. Here, at these synaptic regions astroglial process endings displayed a high degree of dynamic morphological changes. Two defined modes of spontaneous motility could be distinguished: (i) gliding of thin lamellipodia-like membrane protrusions along neuronal surfaces and (ii) transient extensions of filopodia-like processes into the neuronal environment. Our observations highlight the active role of astrocytes in direct modulation of synaptic transmission."],["dc.identifier.doi","10.1111/j.1460-9568.2004.03689.x"],["dc.identifier.isi","000224000800028"],["dc.identifier.pmid","15450103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47430"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0953-816X"],["dc.title","Astroglial processes show spontaneous motility at active synaptic terminals in situ"],["dc.type","journal_article"],["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.artnumber","e4286"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Scheller, Anja"],["dc.contributor.author","Hirrlinger, Petra G."],["dc.contributor.author","Kellert, Beate"],["dc.contributor.author","Tang, Wannan"],["dc.contributor.author","Wehr, Michael C."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Reichenbach, Andreas"],["dc.contributor.author","Sprengel, Rolf"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2019-07-09T11:53:56Z"],["dc.date.available","2019-07-09T11:53:56Z"],["dc.date.issued","2009-01-27"],["dc.description.abstract","Cre/LoxP recombination is the gold standard for conditional gene regulation in mice in vivo. However, promoters driving the expression of Cre recombinase are often active in a wide range of cell types and therefore unsuited to target more specific subsets of cells. To overcome this limitation, we designed inactive ‘‘split-Cre’’ fragments that regain Cre activity when overlapping co-expression is controlled by two different promoters. Using transgenic mice and virus-mediated expression of split-Cre, we show that efficient reporter gene activation is achieved in vivo. In the brain of transgenic mice, we genetically defined a subgroup of glial progenitor cells in which the Plp1- and the Gfap-promoter are simultaneously active, giving rise to both astrocytes and NG2-positive glia. Similarly, a subset of interneurons was labelled after viral transfection using Gad67- and Cck1 promoters to express split-Cre. Thus, split-Cre mediated genomic recombination constitutes a powerful spatial and temporal coincidence detector for in vivo targeting."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0004286"],["dc.identifier.pmid","19172189"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8268"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60531"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Split-Cre Complementation Indicates Coincident Activity of Different Genes In Vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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"]]