Kirchhoff, Frank

[["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","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.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.journal","NEURON GLIA BIOLOGY"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2018-11-07T11:07:14Z"],["dc.date.available","2018-11-07T11:07:14Z"],["dc.date.issued","2007"],["dc.format.extent","S60"],["dc.identifier.isi","000251708800183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52508"],["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","Time-lapse 2-photon laser imaging to study microglia dynamics in the SOD1-mouse model of ALS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]