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.firstpage","1229"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","1241"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Rahman, Jamilur"],["dc.contributor.author","Latal, A. Tobias"],["dc.contributor.author","Besser, Stefanie"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T09:26:26Z"],["dc.date.available","2018-11-07T09:26:26Z"],["dc.date.issued","2013"],["dc.description.abstract","Inhibitory neurons are involved in the generation and patterning of the respiratory rhythm in the adult animal. However, the role of glycinergic neurons in the respiratory rhythm in the developing network is still not understood. Although the complete loss of glycinergic transmission in vivo is lethal, the blockade of glycinergic transmission in slices of the medulla has little effect on pre-Botzinger complex network activity. As 50% of the respiratory rhythmic neurons in this slice preparation are glycinergic, they have to be considered as integrated parts of the network. We aimed to investigate whether glycinergic neurons receive mixed miniature inhibitory postsynaptic currents (mIPSCs) that result from co-release of GABA and glycine. Quantification of mixed mIPSCs by the use of different objective detection methods resulted in a wide range of results. Therefore, we generated traces of mIPSCs with a known distribution of mixed mIPSCs and mono-transmitter-induced mIPSCs, and tested the detection methods on the simulated data. We found that analysis paradigms, which are based on fitting the sum of two mIPSC templates, to be most acceptable. On the basis of these protocols, 2040% of all mIPSCs recorded from respiratory glycinergic neurons are mixed mIPSCs that result from co-release of GABA and glycine. Furthermore, single-cell reverse transcriptase polymerase chain reaction revealed that 46% of glycinergic neurons co-express mRNA of glycine transporter 2 together with at least one marker protein of GABAergic neurons. Our data suggest that significant co-transmission occurs in the pre-Botzinger complex that might be involved in the shaping of synaptic inhibition of respiratory glycinergic neurons."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) [HI1414/2-1, HU797/7-1]; CMPB"],["dc.identifier.doi","10.1111/ejn.12136"],["dc.identifier.isi","000317850800003"],["dc.identifier.pmid","23347272"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30298"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0953-816X"],["dc.title","Mixed miniature postsynaptic currents resulting from co-release of glycine and GABA recorded from glycinergic neurons in the neonatal 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","139"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Vlasov, Alla"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Yin, Dongjiao"],["dc.contributor.author","Nayernia, Karim"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2017-09-07T11:47:33Z"],["dc.date.available","2017-09-07T11:47:33Z"],["dc.date.issued","2009"],["dc.description.abstract","Recently, we reported the successful establishment of multipotent adult germ-Line stem cells (maGSCs) from cultured adult mouse spermatogonial stem cells. Similar to embryonic stem cells, maGSCs are able to self-renew and differentiate into derivatives of all three germ Layers. These properties make maGSCs a potential cell source for the treatment of neural degenerative diseases. In this study, we describe the generation of maGSC-derived proliferating neural precursor cells using growth factor-mediated neural Lineage induction. The neural precursors were positive for nestin and Sox1 and could be continuously expanded. Upon further differentiation, they formed functional neurons and glial cells, as demonstrated by expression of lineage-restricted genes and proteins and by electrophysiological properties. Characterization of maGSC-derived neurons revealed the generation of specific subtypes, including GABAergic, glutamatergic, serotonergic, and dopaminergic neurons. Electrophysiological analysis revealed passive and active membrane properties and postsynaptic currents, indicating their functional maturation. Functional networks formed at later stages of differentiation, as evidenced by synaptic transmission of spontaneous neuronal activity. In conclusion, our data demonstrate that maGSCs may be used as a new stem cell source for basic research and biomedical. applications. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.scr.2008.09.001"],["dc.identifier.gro","3143148"],["dc.identifier.isi","000272224500006"],["dc.identifier.pmid","19383419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/630"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-5061"],["dc.title","Generation of functional neurons and glia from multipotent adult mouse germ-line stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","111"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","347"],["dc.contributor.author","Oku, Yoshitaka"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T10:25:04Z"],["dc.date.available","2018-11-07T10:25:04Z"],["dc.date.issued","2017"],["dc.description.abstract","The topology of the respiratory network in the brainstem has been addressed using different computational models, which help to understand the functional properties of the system. We tested a neural mass model by comparing the result of activation and inhibition of inhibitory neurons in silico with recently published results of optogenetic manipulation of glycinergic neurons [Sherman, et al. (2015) Nat Neurosci 18:408]. The comparison revealed that a five-cell type model consisting of three classes of inhibitory neurons [I-DEC, E-AUG, E-DEC (PI)] and two excitatory populations (pre-I/1) and (I-AUG) neurons can be applied to explain experimental observations made by stimulating or inhibiting inhibitory neurons by light sensitive ion channels. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuroscience.2017.01.041"],["dc.identifier.isi","000398010100011"],["dc.identifier.pmid","28215988"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42776"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1873-7544"],["dc.relation.issn","0306-4522"],["dc.title","A COMPUTATIONAL MODEL OF THE RESPIRATORY NETWORK CHALLENGED AND OPTIMIZED BY DATA FROM OPTOGENETIC MANIPULATION OF GLYCINERGIC NEURONS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","385"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Mesuret, Guillaume"],["dc.contributor.author","Dannenberg, Julia"],["dc.contributor.author","Arnoldt, Mauricio"],["dc.contributor.author","Niebert, Marcus"],["dc.date.accessioned","2018-11-07T10:08:36Z"],["dc.date.available","2018-11-07T10:08:36Z"],["dc.date.issued","2016"],["dc.description.abstract","Mutations in methyl-CpG-binding protein 2 (MECP2) gene have been shown to manifest in a neurodevelopmental disorder that is called Rett syndrome. A typical problem that occurs during development is a disturbance of breathing. To address the role of inhibitory neurons, we generated a mouse line that restores MECP2 in inhibitory neurons in the brainstem by crossbreeding a mouse line that expresses the Cre-recombinase (Cre) in inhibitory neurons under the control of the glycine transporter 2 (GIyT2, slc6a5) promotor(GlyT2-Cre) with a mouse line that has a floxed-stop mutation of the Mecp2 gene (Mecp2(stop/y)). Unrestrained whole-body-plethysmography at postnatal day P60 revealed a low respiratory rate and prolonged respiratory pauses in Mecp2(stop/y) mice. In contrast, G/yT2-Cre positive Mecp2(stop/y) mice (Cre; Mecp2(stop/y)) showed greatly improved respiration and were indistinguishable from wild type littermates. These data support the concept that alterations in inhibitory neurons are important for the development of the respiratory phenotype in Rett syndrome."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.3389/fphys.2016.00385"],["dc.identifier.isi","000382923200001"],["dc.identifier.pmid","27672368"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39494"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","GlyT2-Dependent Preservation of MECP2-Expression in Inhibitory Neurons Improves Early Respiratory Symptoms but Does Not Rescue Survival in a Mouse Model of Rett Syndrome"],["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","797"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","806"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Gomeza, Jesús"],["dc.contributor.author","Ohno, Koji"],["dc.contributor.author","Hülsmann, Swen"],["dc.contributor.author","Armsen, Wencke"],["dc.contributor.author","Eulenburg, Volker"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Laube, Bodo"],["dc.contributor.author","Betz, Heinrich"],["dc.date.accessioned","2019-07-10T08:11:51Z"],["dc.date.available","2019-07-10T08:11:51Z"],["dc.date.issued","2003-11-13"],["dc.description.abstract","The glycine transporter subtype 2 (GlyT2) is localized in the axon terminals of glycinergic neurons. Mice deficient in GlyT2 are normal at birth but during the second postnatal week develop a lethal neuromotor deficiency that resembles severe forms of human hyperekplexia (hereditary startle disease) and is characterized by spasticity, tremor, and an inability to right. Histological and immunological analyses failed to reveal anatomical or biochemical abnormalities, but the amplitudes of glycinergic miniature inhibitory currents (mIPSCs) were strikingly reduced in hypoglossal motoneurons and dissociated spinal neurons from GlyT2-deficient mice. Thus, postnatal GlyT2 function is crucial for efficient transmitter loading of synaptic vesicles in glycinergic nerve terminals, and the GlyT2 gene constitutes a candidate disease gene in human hyperekplexia patients."],["dc.identifier.pmid","14622583"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11248"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60808"],["dc.language.iso","en"],["dc.relation.issn","0896-6273"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.subject.mesh","Amino Acid Transport Systems, Neutral"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Animals, Newborn"],["dc.subject.mesh","Brain Stem"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Fetus"],["dc.subject.mesh","Gene Deletion"],["dc.subject.mesh","Genes, Lethal"],["dc.subject.mesh","Glycine"],["dc.subject.mesh","Glycine Plasma Membrane Transport Proteins"],["dc.subject.mesh","Heredodegenerative Disorders, Nervous System"],["dc.subject.mesh","Hypoglossal Nerve"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Knockout"],["dc.subject.mesh","Motor Neurons"],["dc.subject.mesh","Neural Inhibition"],["dc.subject.mesh","Organ Culture Techniques"],["dc.subject.mesh","Phenotype"],["dc.subject.mesh","Presynaptic Terminals"],["dc.subject.mesh","Startle Reaction"],["dc.subject.mesh","Synaptic Transmission"],["dc.subject.mesh","Synaptic Vesicles"],["dc.title","Deletion of the mouse glycine transporter 2 results in a hyperekplexia phenotype and postnatal lethality."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","The Journal of Physiological Sciences"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Lal, Amit"],["dc.contributor.author","Oku, Yoshitaka"],["dc.contributor.author","Hulsmann, Swen"],["dc.contributor.author","Okada, Yasumasa"],["dc.contributor.author","Miwakeichi, Fumikazu"],["dc.contributor.author","Kawai, Shigeharu"],["dc.contributor.author","Tamura, Yoshiyasu"],["dc.contributor.author","Ishiguro, Makio"],["dc.date.accessioned","2018-11-07T08:34:57Z"],["dc.date.available","2018-11-07T08:34:57Z"],["dc.date.issued","2009"],["dc.format.extent","260"],["dc.identifier.isi","000271023101634"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17944"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Tokyo"],["dc.relation.issn","1880-6546"],["dc.title","NON-DETERMINISTIC BREAKDOWN OF THE PREBOTZINGER COMPLEX NEURONAL SYNCHRONICITY MAY LEAD TO QUANTAL SLOWING OF RESPIRATORY RHYTHM"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","108"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Respiratory Physiology & Neurobiology"],["dc.bibliographiccitation.lastpage","114"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Winter, Stefan M."],["dc.contributor.author","Hirdinger, Johannes"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T10:57:47Z"],["dc.date.available","2018-11-07T10:57:47Z"],["dc.date.issued","2007"],["dc.description.abstract","We screened transgenic mouse lines with Thy 1.2 promoter-induced expression of fluorescent proteins (FPs) for targeting of respiratory neuronal populations in the medulla oblongata. Respiratory neurons were found to be tagged by FPs within the ventral respiratory column (VRC), the pre-Botzinger complex (preBotC) and the rostral ventral respiratory group (rVRG) interneurons. A subset of neurons in the preBotC, labeled with the enhanced yellow fluorescent protein (EYFP), showed inspiratory activity during whole cell recordings from rhythmic slice preparations. Additionally, a subpopulation of EYFP-labeled preBotC neurons expressed both NK1 - and mu-opioid receptors. Furthermore, the spinal tri.-eminal nucleus, the lateral reticular nucleus (LRT) and the hypoglossal nucleus demonstrated intense EYFP expression whereas other regions of the medulla were devoid of neuronal EYFP labeling (e.g. the nucleus ambiguous). In conclusion, Thy 1.2-FP transgenic mice will facilitate the functional analysis of respiratory-related neurons in the medulla and improve the three dimensional analysis of cells contributing to this important neuronal circuit. (c) 2007 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.resp.2007.05.009"],["dc.identifier.isi","000250604200013"],["dc.identifier.pmid","17616445"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50333"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1569-9048"],["dc.title","Transgenic expression of fluorescent proteins in respiratory neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]