Hülsmann, Swen

[["dc.bibliographiccitation.artnumber","e49398"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Hagos, Yohannes"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T09:03:16Z"],["dc.date.available","2018-11-07T09:03:16Z"],["dc.date.issued","2012"],["dc.description.abstract","Sulforhodamine 101 (SR101) is widely used as a marker of astrocytes. In this study we investigated labeling of astrocytes by SR101 in acute slices from the ventrolateral medulla and the hippocampus of transgenic mice expressing EGFP under the control of the astrocyte-specific human GFAP promoter. While SR101 efficiently and specifically labeled EGFP-expressing astrocytes in hippocampus, we found that the same staining procedure failed to label astrocytes efficiently in the ventrolateral medulla. Although carbenoxolone is able to decrease the SR101-labeling of astrocytes in the hippocampus, it is unlikely that SR101 is taken up via gap-junction hemichannels because mefloquine, a blocker for pannexin and connexin hemichannels, was unable to prevent SR101-labeling of hippocampal astrocytes. However, SR101-labeling of the hippocampal astrocytes was significantly reduced by substrates of organic anion transport polypeptides, including estron-3-sulfate and dehydroepiandrosterone sulfate, suggesting that SR101 is actively transported into hippocampal astrocytes."],["dc.identifier.doi","10.1371/journal.pone.0049398"],["dc.identifier.isi","000311929800022"],["dc.identifier.pmid","23189143"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8364"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24870"],["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","Active Sulforhodamine 101 Uptake into Hippocampal Astrocytes"],["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.artnumber","53"],["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Araya Callis, Carolina"],["dc.contributor.author","Flügge, Gabriele"],["dc.contributor.author","Hülsmann, Swen"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:22:20Z"],["dc.date.available","2018-09-28T10:22:20Z"],["dc.date.issued","2012"],["dc.description.abstract","Chronic stress affects neuronal networks by inducing dendritic retraction, modifying neuronal excitability and plasticity, and modulating glial cells. To elucidate the functional consequences of chronic stress for the hippocampal network, we submitted adult rats to daily restraint stress for 3 weeks (6 h/day). In acute hippocampal tissue slices of stressed rats, basal synaptic function and short-term plasticity at Schaffer collateral/CA1 neuron synapses were unchanged while long-term potentiation was markedly impaired. The spatiotemporal propagation pattern of hypoxia-induced spreading depression episodes was indistinguishable among control and stress slices. However, the duration of the extracellular direct current potential shift was shortened after stress. Moreover, K(+) fluxes early during hypoxia were more intense, and the postsynaptic recoveries of interstitial K(+) levels and synaptic function were slower. Morphometric analysis of immunohistochemically stained sections suggested hippocampal shrinkage in stressed rats, and the number of cells that are immunoreactive for glial fibrillary acidic protein was increased in the CA1 subfield indicating activation of astrocytes. Western blots showed a marked downregulation of the inwardly rectifying K(+) channel Kir4.1 in stressed rats. Yet, resting membrane potentials, input resistance, and K(+)-induced inward currents in CA1 astrocytes were indistinguishable from controls. These data indicate an intensified interstitial K(+) accumulation during hypoxia in the hippocampus of chronically stressed rats which seems to arise from a reduced interstitial volume fraction rather than impaired glial K(+) buffering. One may speculate that chronic stress aggravates hypoxia-induced pathophysiological processes in the hippocampal network and that this has implications for the ischemic brain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.3389/fphar.2012.00053"],["dc.identifier.pmid","22470344"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7501"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15856"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1663-9812"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Restraint Stress Intensifies Interstitial K(+) Accumulation during Severe Hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","193"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Structure and Function"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","220"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Shahmoradi, Ali"],["dc.contributor.author","Wichert, Sven P."],["dc.contributor.author","Mayerl, Steffen"],["dc.contributor.author","Hagos, Yohannes"],["dc.contributor.author","Heuer, Heike"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T10:03:38Z"],["dc.date.available","2018-11-07T10:03:38Z"],["dc.date.issued","2015"],["dc.description.abstract","Sulforhodamine 101 (SR101) is widely used for astrocyte identification, though the labeling mechanism remains unknown and the efficacy of labeling in different brain regions is heterogeneous. By combining region-specific isolation of astrocytes followed by transcriptome analysis, two-photon excitation microscopy, and mouse genetics, we identified the thyroid hormone transporter OATP1C1 as the SR101-uptake transporter in hippocampus and cortex."],["dc.identifier.doi","10.1007/s00429-013-0645-0"],["dc.identifier.isi","000348980800014"],["dc.identifier.pmid","24129767"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38516"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1863-2661"],["dc.relation.issn","1863-2653"],["dc.title","The multispecific thyroid hormone transporter OATP1C1 mediates cell-specific sulforhodamine 101-labeling of hippocampal astrocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","18"],["dc.bibliographiccitation.journal","Respiratory Physiology & Neurobiology"],["dc.bibliographiccitation.lastpage","23"],["dc.bibliographiccitation.volume","226"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Negm, Mahmoud"],["dc.contributor.author","Driehaus, Johannes"],["dc.contributor.author","Scheller, Anja"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T10:13:58Z"],["dc.date.available","2018-11-07T10:13:58Z"],["dc.date.issued","2016"],["dc.description.abstract","The neuronal activity in the respiratory network of the ventrolateral medulla strongly depends on a variety of different neuromodulators. Since the respiratory activity generated by neurons in the pre-Botzinger complex (preBotC) is stabilized by astrocytes, we investigated potential effects of the neuromodulator norepinephrine (NE) on the astrocytic calcium signaling in the ventral respiratory group. In acutely isolated brainstem slices from wild type mice (postnatal day 1-10) we performed calcium imaging experiments using Oregon Green 488 BAPTA-1 AM as a calcium indicator dye. Astrocytes in the preBotC, which were identified by their unique intracellular calcium rise after the reduction of the extracellular K+ concentration, showed calcium rises in response to norepinephrine. These calcium signals persisted after blockade of neuronal activity by tetrodotoxin (TTX) indicating that they were independent of neuronal activity. Furthermore, application of the endoplasmic reticulum calcium pump blocker cyclopiazonic acid (CPA) diminished norepinephrine-induced calcium signals. This results could be confirmed using trans genic mice with astrocyte specific expression of GCaMP3. Thus, norepinephrine might, apart from acting directly on neurons, influence and modulate respiratory network activity via the modulation of astroglial calcium signaling. (C) 2015 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.resp.2015.10.008"],["dc.identifier.isi","000375515800004"],["dc.identifier.pmid","26514085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40532"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1878-1519"],["dc.relation.issn","1569-9048"],["dc.title","Norepinephrine-induced calcium signaling in astrocytes in the respiratory network of the ventrolateral medulla"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","815"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","827"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Haertel, Kai"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T08:29:17Z"],["dc.date.available","2018-11-07T08:29:17Z"],["dc.date.issued","2009"],["dc.description.abstract","A controlled, periodic exchange of air between lungs and atmosphere requires a neuronal rhythm generated by a network of neurons in the ventral respiratory group (VRG) of the brainstem. Glial cells, e.g. astrocytes, have been shown to be supportive in stabilizing this neuronal activity in the central nervous system during development. In addition, a variety of neuromodulators including serotonin (5-HT), Substance P (SP), and thyrotropin-releasing hormone (TRH) stimulate respiratory neurons directly. If astrocytes in the VRG, like their neuronal neighbors, are also directly stimulated by neuromodulators, they might indirectly affect the respiratory neurons and consequently the respiratory rhythm. In the present study, we provide support for this concept by demonstrating expression of NK1-R, TRH-R, and 5-HT(2)-R in astrocytes of the VRG with immunohistochemistry. Additionally, we showed that the external application of the neuromodulators 5-HT, SP, and TRH activate calcium transients in VRG astrocytes. Consequently, we postulate that in the VRG of the neonatal mouse, neuromodulation by SP, TRH, and serotonin also involves astrocytic calcium signaling. (C) 2008 Wiley-Liss, Inc."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG)"],["dc.identifier.doi","10.1002/glia.20808"],["dc.identifier.isi","000265572300002"],["dc.identifier.pmid","19031447"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16613"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","Astrocytic Calcium Signals Induced by Neuromodulators via Functional Metabotropic Receptors in the Ventral Respiratory Group of Neonatal Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","97"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.seriesnr","669"],["dc.contributor.author","Winter, Stefan M."],["dc.contributor.author","Fresemann, Jens"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Oku, Yoshitaka"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T08:48:16Z"],["dc.date.available","2018-11-07T08:48:16Z"],["dc.date.issued","2010"],["dc.description.abstract","The neuronal network in the pre-Botzinger Complex is the key element of respiratory rhythm generation. Isolated in a slice preparation, the pre-Botzinger Complex network is still able to generate its inspiratory activity. Although the mechanism of rhythm generation in principle relies on glutamatergic neurons, interestingly we found that glycinergic neurons represent a major portion of all inspiratory neurons in the slice preparation."],["dc.identifier.doi","10.1007/978-1-4419-5692-7_20"],["dc.identifier.isi","000277995200020"],["dc.identifier.pmid","20217329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21163"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Berlin"],["dc.relation.conference","11th Oxford Conference on Modeling and Control of Breathing"],["dc.relation.crisseries","Advances in Experimental Medicine and Biology"],["dc.relation.eventend","2009-07-26"],["dc.relation.eventlocation","Nara, Japan"],["dc.relation.eventstart","2009-07-23"],["dc.relation.isbn","978-1-4419-5691-0"],["dc.relation.ispartof","New frontiers in respiratory control"],["dc.relation.ispartofseries","Advances in Experimental Medicine and Biology; 669"],["dc.title","Glycinergic Interneurons in the Respiratory Network of the Rhythmic Slice Preparation"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","459"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Pflügers Archiv - European Journal of Physiology"],["dc.bibliographiccitation.lastpage","469"],["dc.bibliographiccitation.volume","458"],["dc.contributor.author","Winter, Stefan M."],["dc.contributor.author","Fresemann, Jens"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Oku, Yoshitaka"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T08:28:29Z"],["dc.date.available","2018-11-07T08:28:29Z"],["dc.date.issued","2009"],["dc.description.abstract","Neuronal activity in the respiratory network is functionally dependent on inhibitory synaptic transmission. Using two-photon excitation microscopy, we analyzed the integration of glycinergic neurons in the isolated inspiratory pre-Botzinger complex-driven network of the rhythmic slice preparation. Inspiratory (96%) and 'tonic' expiratory neurons (4%) were identified via an increase or decrease, respectively, of the cytosolic free calcium concentration during the inspiratory-related respiratory burst. Furthermore, in BAC-transgenic mice expressing EGFP under the control of the GlyT2-promoter, 50% of calcium-imaged inspiratory neurons were glycinergic. Inspiratory bursting of glycinergic neurons in the slice was confirmed by whole-cell recording. We also found glycinergic neurons that receive phasic inhibition from other glycinergic neurons. Our calcium imaging data show that glycinergic neurons comprise a large population of inspiratory neurons in the pre-Botzinger complex-driven network of the rhythmic slice preparation."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.1007/s00424-009-0647-1"],["dc.identifier.isi","000266789000002"],["dc.identifier.pmid","19238427"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16432"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0031-6768"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Glycinergic interneurons are functionally integrated into the inspiratory network of mouse medullary slices"],["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.firstpage","1"],["dc.bibliographiccitation.journal","Brain Structure and Function"],["dc.bibliographiccitation.lastpage","26"],["dc.contributor.author","Rahman, Jamilur"],["dc.contributor.author","Besser, Stefanie"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Eulenburg, Volker"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Wojcik, Sonja M."],["dc.contributor.author","Hülsmann, Swen"],["dc.date.accessioned","2019-07-09T11:41:21Z"],["dc.date.available","2019-07-09T11:41:21Z"],["dc.date.issued","2014"],["dc.description.abstract","Both glycinergic and GABAergic neurons require the vesicular inhibitory amino acid transporter (VIAAT) for synaptic vesicle filling. Presynaptic GABA concentrations are determined by the GABA synthesizing enzymes glutamate decarboxylase (GAD)65 and GAD67, whereas the presynaptic glycine content depends on the plasma membrane glycine transporter 2 (GlyT2). Although severely impaired, glycinergic transmission is not completely absent in GlyT2-knockout mice, suggesting that other routes of glycine uptake or de novo synthesis of glycine exist in presynaptic terminals. To investigate the consequences of a complete loss of glycinergic transmission, we generated a mouse line with a conditional ablation of VIAAT in glycinergic neurons by crossing mice with loxP-flanked VIAAT alleles with a GlyT2-Cre transgenic mouse line. Interestingly, conditional VIAAT knockout (VIAAT cKO) mice were not viable at birth. In addition to the dominant respiratory failure, VIAAT cKO showed an umbilical hernia and a cleft palate. Immunohistochemistry revealed an almost complete depletion of VIAAT in the brainstem. Electrophysiology revealed the absence of both spontaneous glycinergic and GABAergic inhibitory postsynaptic currents (IPSCs) from hypoglossal motoneurons. Our results demonstrate that the deletion of VIAAT in GlyT2-Cre expressing neurons also strongly affects GABAergic transmission and suggest a large overlap of the glycinergic and the GABAergic neuron population during early development in the caudal parts of the brain."],["dc.identifier.doi","10.1007/s00429-014-0829-2"],["dc.identifier.pmid","25027639"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11988"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58409"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Genetic ablation of VIAAT in glycinergic neurons causes a severe respiratory phenotype and perinatal death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","submitted_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Hagos, Yohannes"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T09:23:24Z"],["dc.date.available","2018-11-07T09:23:24Z"],["dc.date.issued","2013"],["dc.format.extent","S120"],["dc.identifier.isi","000320408400380"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29568"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","11th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","DEHYDROEPIANDROSTERONE SULFATE AND SULFORHODAMINE 101 COMPETE FOR ACTIVE UPTAKE BY AN ORGANIC ANION TRANSPORTING POLYPEPTIDE IN HIPPOCAMPAL ASTROCYTES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e26309"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Fresemann, Jens"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T08:50:41Z"],["dc.date.available","2018-11-07T08:50:41Z"],["dc.date.issued","2011"],["dc.description.abstract","Respiratory neuronal network activity is thought to require efficient functioning of astrocytes. Here, we analyzed neuronastrocyte communication in the pre-Botzinger Complex (preBotC) of rhythmic slice preparations from neonatal mice. In astrocytes that exhibited rhythmic potassium fluxes and glutamate transporter currents, we did not find a translation of respiratory neuronal activity into phase-locked astroglial calcium signals. In up to 20% of astrocytes, 2-photon calcium imaging revealed spontaneous calcium fluctuations, although with no correlation to neuronal activity. Calcium signals could be elicited in preBotC astrocytes by metabotropic glutamate receptor activation or after inhibition of glial glutamate uptake. In the latter case, astrocyte calcium elevation preceded a surge of respiratory neuron discharge activity followed by network failure. We conclude that astrocytes do not exhibit respiratory-rhythmic calcium fluctuations when they are able to prevent synaptic glutamate accumulation. Calcium signaling is, however, observed when glutamate transport processes in astrocytes are suppressed or neuronal discharge activity is excessive."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [CMPB, SPP1172]"],["dc.identifier.doi","10.1371/journal.pone.0026309"],["dc.identifier.isi","000296507500048"],["dc.identifier.pmid","22039458"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21749"],["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","Determinants of Functional Coupling between Astrocytes and Respiratory Neurons in the Pre-Botzinger Complex"],["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"]]