Kirchhoff, Frank

[["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.firstpage","2431"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","2440"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Schomburg, Eike D."],["dc.date.accessioned","2018-11-07T08:40:21Z"],["dc.date.available","2018-11-07T08:40:21Z"],["dc.date.issued","2010"],["dc.description.abstract","As CNS macrophages, microglia show a high spontaneous motility of their processes, continuously surveying their microenvironment. Upon CNS injury, microglia react by immediate cellular polarization and process extension toward the lesion site as well as by subsequent amoeboid lesion-directed migration and phagocytosis. To determine the ability of microglia to fulfill their role within distinctively lesioned tissue in the absence of life support, we investigated microglial activity and responsiveness to laser-induced axonal injuries in the spinal dorsal columns in situ after cardiac and respiratory arrest, i.e., post-mortem, in the progressively degrading nervous tissue. For this purpose, we used time-lapse two-photon laser scanning microscopy in double transgenic mice expressing enhanced green fluorescent protein in microglia and enhanced yellow fluorescent protein in projection neurons. Depending on the premortal condition of the animal, microglial activity and responsiveness remain for up to 5-10 hr post-mortem. Thereby, the continuously decreasing glial reaction is independent of oxygen and glucose supply but requires residual ATP, suggesting a parasitic form of energy, such as a transmembrane uptake of ATP released from injured nervous tissue. Even though initially microglia are able to detect axonal injury after disruption of the blood supply, the later aspects of glial reaction, for example amoeboid conversion and migration, are absent postmortem, corresponding to the failure of microglia to prevent secondary damage after injury of nervous tissue. (C) 2010 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jnr.22402"],["dc.identifier.isi","000280436600012"],["dc.identifier.pmid","20623536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19215"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0360-4012"],["dc.title","Long-Lasting Post-Mortem Activity of Spinal Microglia In Situ in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","151"],["dc.bibliographiccitation.volume","497"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2018-11-07T08:54:58Z"],["dc.date.available","2018-11-07T08:54:58Z"],["dc.date.issued","2011"],["dc.description.abstract","Pathophysiology of the motoneuron disease amyotrophic lateral sclerosis (ALS) is non-cell-autonomous. In mouse models of familiar ALS, neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring glial cells. In vivo imaging by two-photon laser-scanning microscopy was used to study rapid morphological reactions of astroglial cells towards laser-induced axonal transection in ALS-linked transgenic SOD1(G93A) mice. In the affected lateral spinal cord, mutated astroglial cells extended branches towards injured axons within a time frame of minutes to hours post lesion while in control animals astrocytes lack any rapid morphological alteration within the studied time frame. This suggests that astrocytes partially contribute to the rapid response of non-neuronal cells to acute axonal lesions in ALS mice. (C) 2011 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2011.04.049"],["dc.identifier.isi","000292404400016"],["dc.identifier.pmid","21539893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22797"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","In vivo imaging reveals rapid morphological reactions of astrocytes towards focal lesions in an ALS mouse model"],["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","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","107"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","109"],["dc.bibliographiccitation.volume","487"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Schomburg, Eike D."],["dc.date.accessioned","2018-11-07T09:00:09Z"],["dc.date.available","2018-11-07T09:00:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Functional relevance of non-synaptic purinergic receptors on dorsal root ganglion cells was tested in vivo by the influence of ATP using 2P-LSM and Ca imaging. Within a few seconds after local application of ATP, neurones in dorsal root ganglion were activated indicated by an increase of their calcium signal. The signal reached its maximum within a few seconds and declined to control values after about 30s. Purinergic action seems to include non-synaptic cell-to-cell communication within dorsal root ganglia. (C) 2010 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","DFG [Scho 37/16]"],["dc.identifier.doi","10.1016/j.neulet.2010.10.005"],["dc.identifier.isi","000285495100024"],["dc.identifier.pmid","20937358"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24082"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Purinergic activation of dorsal root ganglion neurones in vivo"],["dc.type","journal_article"],["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.artnumber","e17910"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2018-11-07T08:58:04Z"],["dc.date.available","2018-11-07T08:58:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Mutations in the enzyme superoxide dismutase-1 (SOD1) cause hereditary variants of the fatal motor neuronal disease Amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous: neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring non-neuronal cells. In vivo imaging by two-photon laser-scanning microscopy was used to compare the role of microglia/macrophage-related neuroinflammation in the CNS and PNS using ALS-linked transgenic SOD1(G93A) mice. These mice contained labeled projection neurons and labeled microglia/macrophages. In the affected lateral spinal cord (in contrast to non-affected dorsal columns), different phases of microglia-mediated inflammation were observed: highly reactive microglial cells in preclinical stages (in 60-day-old mice the reaction to axonal transection was similar to 180% of control) and morphologically transformed microglia that have lost their function of tissue surveillance and injury-directed response in clinical stages (reaction to axonal transection was lower than 50% of control). Furthermore, unlike CNS microglia, macrophages of the PNS lack any substantial morphological reaction while preclinical degeneration of peripheral motor axons and neuromuscular junctions was observed. We present in vivo evidence for a different inflammatory activity of microglia and macrophages: an aberrant neuroinflammatory response of microglia in the CNS and an apparently mainly neurodegenerative process in the PNS."],["dc.identifier.doi","10.1371/journal.pone.0017910"],["dc.identifier.isi","000288545100043"],["dc.identifier.pmid","21437247"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23554"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","In Vivo Imaging Reveals Distinct Inflammatory Activity of CNS Microglia versus PNS Macrophages in a Mouse Model for ALS"],["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"]]

[["dc.bibliographiccitation.journal","The Journal of Physiological Sciences"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2018-11-07T08:34:57Z"],["dc.date.available","2018-11-07T08:34:57Z"],["dc.date.issued","2009"],["dc.format.extent","199"],["dc.identifier.isi","000271023101265"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17943"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Tokyo"],["dc.relation.issn","1880-6546"],["dc.title","LONG LASTING POST MORTEM ACTIVITY OF MICROGLIA IN SITU 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"]]