Stühmer, Walter

[["dc.bibliographiccitation.firstpage","194"],["dc.bibliographiccitation.journal","Journal of Neuroscience Methods"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Samhaber, Robert"],["dc.contributor.author","Schottdorf, Manuel"],["dc.contributor.author","El Hady, Ahmed"],["dc.contributor.author","Broeking, Kai"],["dc.contributor.author","Daus, Andreas"],["dc.contributor.author","Thielemann, Christiane"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Wolf, Fred"],["dc.date.accessioned","2018-11-07T10:19:24Z"],["dc.date.available","2018-11-07T10:19:24Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Multi-electrode arrays (MEAs) allow non-invasive multi-unit recording in-vitro from cultured neuronal networks. For sufficient neuronal growth and adhesion on such MEAs, substrate preparation is required. Plating of dissociated neurons on a uniformly prepared MEA's surface results in the formation of spatially extended random networks with substantial inter-sample variability. Such cultures are not optimally suited to study the relationship between defined structure and dynamics in neuronal networks. To overcome these shortcomings, neurons can be cultured with pre-defined topology by spatially structured surface modification. Spatially structuring a MEA surface accurately and reproducibly with the equipment of a typical cell-culture laboratory is challenging. New method: In this paper, we present a novel approach utilizing micro-contact printing (mu CP) combined with a custom-made device to accurately position patterns on MEAs with high precision. We call this technique AP-mu CP (accurate positioning micro-contact printing). Comparison with existing methods: Other approaches presented in the literature using mu CP for patterning either relied on facilities or techniques not readily available in a standard cell culture laboratory, or they did not specify means of precise pattern positioning. Conclusion: Here we present a relatively simple device for reproducible and precise patterning in a standard cell-culture laboratory setting. The patterned neuronal islands on MEAs provide a basis for high throughput electrophysiology to study the dynamics of single neurons and neuronal networks. (C) 2015 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneumeth.2015.09.022"],["dc.identifier.isi","000366224100020"],["dc.identifier.pmid","26432934"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41649"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1872-678X"],["dc.relation.issn","0165-0270"],["dc.title","Growing neuronal islands on multi-electrode arrays using an accurate positioning-mu CP device"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e2114549118"],["dc.bibliographiccitation.issue","51"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Merino, Ricardo Martins"],["dc.contributor.author","Leon-Pinzon, Carolina"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Möck, Martin"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Wolf, Fred"],["dc.contributor.author","Neef, Andreas"],["dc.date.accessioned","2022-02-01T10:31:17Z"],["dc.date.available","2022-02-01T10:31:17Z"],["dc.date.issued","2021"],["dc.description.abstract","Fast oscillations in cortical circuits critically depend on GABAergic interneurons. Which interneuron types and populations can drive different cortical rhythms, however, remains unresolved and may depend on brain state. Here, we measured the sensitivity of different GABAergic interneurons in prefrontal cortex under conditions mimicking distinct brain states. While fast-spiking neurons always exhibited a wide bandwidth of around 400 Hz, the response properties of spike-frequency adapting interneurons switched with the background input\\’s statistics. Slowly fluctuating background activity, as typical for sleep or quiet wakefulness, dramatically boosted the neurons\\’ sensitivity to gamma and ripple frequencies. We developed a time-resolved dynamic gain analysis and revealed rapid sensitivity modulations that enable neurons to periodically boost gamma oscillations and ripples during specific phases of ongoing low-frequency oscillations. This mechanism predicts these prefrontal interneurons to be exquisitely sensitive to high-frequency ripples, especially during brain states characterized by slow rhythms, and to contribute substantially to theta-gamma cross-frequency coupling."],["dc.description.abstract","Fast oscillations in cortical circuits critically depend on GABAergic interneurons. Which interneuron types and populations can drive different cortical rhythms, however, remains unresolved and may depend on brain state. Here, we measured the sensitivity of different GABAergic interneurons in prefrontal cortex under conditions mimicking distinct brain states. While fast-spiking neurons always exhibited a wide bandwidth of around 400 Hz, the response properties of spike-frequency adapting interneurons switched with the background input’s statistics. Slowly fluctuating background activity, as typical for sleep or quiet wakefulness, dramatically boosted the neurons’ sensitivity to gamma and ripple frequencies. We developed a time-resolved dynamic gain analysis and revealed rapid sensitivity modulations that enable neurons to periodically boost gamma oscillations and ripples during specific phases of ongoing low-frequency oscillations. This mechanism predicts these prefrontal interneurons to be exquisitely sensitive to high-frequency ripples, especially during brain states characterized by slow rhythms, and to contribute substantially to theta-gamma cross-frequency coupling."],["dc.identifier.doi","10.1073/pnas.2114549118"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98819"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.rights.uri","https://www.pnas.org/site/aboutpnas/licenses.xhtml"],["dc.title","Theta activity paradoxically boosts gamma and ripple frequency sensitivity in prefrontal interneurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","589"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","598"],["dc.bibliographiccitation.volume","171"],["dc.contributor.author","Herrero-Herranz, Eva"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T10:59:44Z"],["dc.date.available","2018-11-07T10:59:44Z"],["dc.date.issued","2007"],["dc.description.abstract","Mechanisms of lesion repair in multiple sclerosis are incompletely understood. To some degree, remyelination can occur, associated with an increase of proliferating oligodendroglial cells. Recently, the expression of potassium channels has been implicated in the control of oligodendrocyte precursor cell proliferation in vitro. We investigated the expression of Kv1.4 potassium channels in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Confocal microscopy revealed expression of Kv1.4 in AN2-positive oligodendrocyte precursor cells and pre-myelinating oligodendrocytes in vitro but neither in mature oligodendrocytes nor in the spinal cords of healthy adult mice. After induction of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, Kv1.4 immunoreactivity was detected in or around lesions already during disease onset with a peak early and a subsequent decrease in the late phase of the disease. Kv1.4 expression was confined to 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive oligodendroglial cells, which were actively proliferating and ensheathed naked axons. After a demyelinating episode, the number of Kv1.4 and 2',3'-cyclic nucleotide 3'-phosphodiesterase double-positive cells was greatly reduced in ciliary neurotrophic factor knockout mice, a model with impaired lesion repair. in summary, the re-expression of an oligodendroglial potassium channel may have a functional implication on oligodendroglial cell cycle progression, thus influencing tissue repair in experimental autoimmune encephalomyelitis and multiple sclerosis."],["dc.identifier.doi","10.2353/ajpath.2007.061241"],["dc.identifier.isi","000248496300022"],["dc.identifier.pmid","17600124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50766"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0002-9440"],["dc.title","Re-expression of a developmentally restricted potassium channel in autoimmune demyelination - Kv1.4 is implicated in oligodendroglial proliferation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","846"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","853"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Becherer, U."],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Oheim, M."],["dc.date.accessioned","2017-09-07T11:44:20Z"],["dc.date.available","2017-09-07T11:44:20Z"],["dc.date.issued","2003"],["dc.description.abstract","Ca2+ microdomains that form during the opening of voltage-gated Ca2+ channels have been implicated in regulating the kinetics of hormone and transmitter release. Direct assessment of the interaction between a single Ca2+ microdomain and a single secretory vesicle has been impossible because of technical limitations. Using evanescent field imaging of near-membrane micromolar Ca2+ concentration ([Ca2+]) and fluorescently labeled vesicles, we have observed exocytosis of individual chromaffin dense-core vesicles that was triggered by Ca2+ microdomains. Ca2+ microdomains selectively triggered the release of vesicles that were docked within 300 nm. Not all vesicles exposed to a Ca2+ microdomain were released, indicating that some vesicles are docked but are not ready for release. In addition to its established role as a trigger for release, elevated near-membrane [Ca2+] reduced the distance between docked vesicles and Ca2+ entry sites. Our results suggest a new mechanism for stimulation-dependent facilitation of exocytosis, whereby vesicles are moved closer to Ca2+ entry sites, thereby increasing a Ca2+ microdomain's efficacy to trigger vesicle fusion."],["dc.identifier.doi","10.1038/nn1087"],["dc.identifier.gro","3144079"],["dc.identifier.isi","000184413700014"],["dc.identifier.pmid","12845327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1663"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1097-6256"],["dc.title","Calcium regulates exocytosis at the level of single vesicles"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2850"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","2852"],["dc.bibliographiccitation.volume","580"],["dc.contributor.author","Stuhmer, Walter"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Hartung, Franziska"],["dc.contributor.author","Zientkowska, M."],["dc.contributor.author","Pardo, L. A."],["dc.date.accessioned","2018-11-07T09:48:45Z"],["dc.date.available","2018-11-07T09:48:45Z"],["dc.date.issued","2006"],["dc.description.abstract","An increasing number of ion channels are being found to be causally involved in diseases, giving rise to the new field of \"channelopathies\". Cancer is no exception, and several ion channels have been linked to tumour progression. Among them is the potassium channel EAG (Ether-a-go-go). Over 75% of tumours have been tested positive using a monoclonal antibody specific for EAG, while inhibition of this channel decreased the proliferation of EAG expressing cells. The inhibition of EAG is accomplished using RNA interference, functional anti-EAG1 antibodies, or (unspecific) EAG channel blockers. Fluorescently labelled recombinant Fab fragments recognizing EAG allow the distribution of EAG to be visualized in an in vivo mouse tumour model. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.febslet.2006.03.062"],["dc.identifier.isi","000238167200009"],["dc.identifier.pmid","16783874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35368"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0014-5793"],["dc.title","Potassium channels as tumour markers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","261"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Proteomics"],["dc.bibliographiccitation.lastpage","269"],["dc.contributor.author","Sussulini, Alessandra"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Muller Banzato, Claudio Eduardo"],["dc.contributor.author","Zezzi Arruda, Marco Aurelio"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Kratzin, Hartmut D."],["dc.date.accessioned","2017-09-07T11:46:27Z"],["dc.date.available","2017-09-07T11:46:27Z"],["dc.date.issued","2011"],["dc.description.abstract","The molecular basis of bipolar disorder (BD) is still unknown as is the mechanism through which lithium, the therapy of choice, exerts its effects in treatment of BD. So far, no biomarkers exist to facilitate diagnosis of BD or treatment evaluation. To investigate whether BD and its treatment with lithium leaves a characteristic signature in the serum proteome, we used SELDI-TOF MS to analyze individual serum samples from BD patients treated with lithium (BD-plus-Li, n=15) or other drugs (BD-minus-Li, n=10) and from healthy controls (n=15). Interestingly, features of 28 kDa (one peak) and 14 kDa (three peaks) showed a decreased level in the BD-minus-Li group and a level restored to that of the control group in the BD-plus-Li group. To reveal the identity of these features, we subjected pooled serum samples from both BD groups to the 2-D DIGE technology and identified 28 kDa apolipoprotein A-I (apo A-I) and three 14 kDa fragments thereof as upregulated in the BD-plus-Li group. Immunoturbidimetry, a routine clinical assay, verified the characteristic apo A-I signature in individual serum samples. In conclusion, we propose apo A-I as a candidate marker that can visualize response to lithium treatment at the serum protein level."],["dc.identifier.doi","10.1002/pmic.201000371"],["dc.identifier.gro","3150515"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7288"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Apolipoprotein A-I as a candidate serum marker for the response to lithium treatment in bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2247"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","2262"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Ufartes, Roser"],["dc.contributor.author","Schneider, Tomasz"],["dc.contributor.author","Mortensen, Lena Suenke"],["dc.contributor.author","de Juan Romero, Camino"],["dc.contributor.author","Hentrich, Klaus"],["dc.contributor.author","Knoetgen, Hendrik"],["dc.contributor.author","Beilinson, Vadim"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Rawlins, J. Nicholas P."],["dc.contributor.author","Stühmer, Walter"],["dc.date.accessioned","2018-11-07T09:24:20Z"],["dc.date.available","2018-11-07T09:24:20Z"],["dc.date.issued","2013"],["dc.description.abstract","K(v)10.1 (Eag1), member of the K(v)10 family of voltage-gated potassium channels, is preferentially expressed in adult brain. The aim of the present study was to unravel the functional role of K(v)10.1 in the brain by generating knockout mice, where the voltage sensor and pore region of K(v)10.1 were removed to render non-functional proteins through deletion of exon 7 of the KCNH1 gene using the '3 Lox P strategy'. K(v)10.1-deficient mice show no obvious alterations during embryogenesis and develop normally to adulthood; cortex, hippocampus and cerebellum appear anatomically normal. Other tests, including general health screen, sensorimotor functioning and gating, anxiety, social behaviour, learning and memory did not show any functional aberrations in K(v)10.1 null mice. K(v)10.1 null mice display mild hyperactivity and longer-lasting haloperidol-induced catalepsy, but there was no difference between genotypes in amphetamine sensitization and withdrawal, reactivity to apomorphine and haloperidol in the prepulse inhibition tests or to antidepressants in the haloperidol-induced catalepsy. Furthermore, electrical properties of K(v)10.1 in cerebellar Purkinje cells did not show any difference between genotypes. Bearing in mind that K(v)10.1 is overexpressed in over 70 of all human tumours and that its inhibition leads to a reduced tumour cell proliferation, the fact that deletion of K(v)10.1 does not show a marked phenotype is a prerequisite for utilizing K(v)10.1 blocking and/or reduction techniques, such as siRNA, to treat cancer."],["dc.description.sponsorship","Max Planck Society"],["dc.identifier.doi","10.1093/hmg/ddt076"],["dc.identifier.isi","000319432000011"],["dc.identifier.pmid","23424202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29798"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0964-6906"],["dc.title","Behavioural and functional characterization of K(v)10.1 (Eag1) knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","675"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Current Medicinal Chemistry"],["dc.bibliographiccitation.lastpage","682"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Pardo, L. A."],["dc.contributor.author","Gomez-Varela, David"],["dc.contributor.author","Major, Felix"],["dc.contributor.author","Sansuk, K."],["dc.contributor.author","Leurs, R."],["dc.contributor.author","Downie, B. R."],["dc.contributor.author","Tietze, Lutz Friedjan"],["dc.contributor.author","Stühmer, Walter"],["dc.date.accessioned","2018-11-07T09:13:48Z"],["dc.date.available","2018-11-07T09:13:48Z"],["dc.date.issued","2012"],["dc.description.abstract","K(V)10.1 has recently become generally accepted as a promising cancer target, as it is ectopically expressed in the majority of solid tumors. Due to its cell-surface accessibility, K(V)10.1 has a strong potential for tumor treatment and diagnosis. Given that its mode of action is likely independent of conventional cancer pathways such as tyrosine kinases, K(V)10.1 opens a novel window for treating cancer. In this review we will give an overview of the current status of data linking K(V)10.1 to cancer, and propose techniques that could exploit K(V)10.1's properties for the management of cancer."],["dc.identifier.isi","000300443700005"],["dc.identifier.pmid","22204340"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27252"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0929-8673"],["dc.title","Approaches Targeting K(V)10.1 Open a Novel Window for Cancer Diagnosis and Therapy"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","115"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Membrane Biology"],["dc.bibliographiccitation.lastpage","124"],["dc.bibliographiccitation.volume","205"],["dc.contributor.author","Pardo, L.A."],["dc.contributor.author","Contreras-Jurado, C."],["dc.contributor.author","Zientkowska, M."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Stühmer, W."],["dc.date.accessioned","2022-03-01T11:44:27Z"],["dc.date.available","2022-03-01T11:44:27Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1007/s00232-005-0776-1"],["dc.identifier.pii","776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103030"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1432-1424"],["dc.relation.issn","0022-2631"],["dc.title","Role of Voltage-gated Potassium Channels in Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Samhaber, Robert"],["dc.contributor.author","Schottdorf, Manuel"],["dc.contributor.author","Hady, Ahmed El"],["dc.contributor.author","Broeking, Kai"],["dc.contributor.author","Daus, Andreas"],["dc.contributor.author","Thielemann, Christiane"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Wolf, Fred"],["dc.date.accessioned","2017-09-07T11:45:41Z"],["dc.date.available","2017-09-07T11:45:41Z"],["dc.date.issued","2015"],["dc.identifier.gro","3151836"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8663"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.publisher","Cold Spring Harbor Laboratory"],["dc.title","Growing neuronal islands on multi-electrode arrays using an Accurate Positioning-μCP device"],["dc.type","preprint"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]