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.journal","Frontiers in Neural Circuits"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","El Hady, Ahmed"],["dc.contributor.author","Afshar, Ghazaleh"],["dc.contributor.author","Bröking, Kai"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Geisel, Theo"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Wolf, Fred"],["dc.date.accessioned","2017-09-07T11:45:38Z"],["dc.date.available","2017-09-07T11:45:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Synchronized bursting is found in many brain areas and has also been implicated in the pathophysiology of neuropsychiatric disorders such as epilepsy, Parkinson’s disease, and schizophrenia. Despite extensive studies of network burst synchronization, it is insufficiently understood how this type of network wide synchronization can be strengthened, reduced, or even abolished. We combined electrical recording using multi-electrode array with optical stimulation of cultured channelrhodopsin-2 transducted hippocampal neurons to study and manipulate network burst synchronization. We found low frequency photo-stimulation protocols that are sufficient to induce potentiation of network bursting, modifying bursting dynamics, and increasing interneuronal synchronization. Surprisingly, slowly fading-in light stimulation, which substantially delayed and reduced light-driven spiking, was at least as effective in reorganizing network dynamics as much stronger pulsed light stimulation. Our study shows that mild stimulation protocols that do not enforce particular activity patterns onto the network can be highly effective inducers of network-level plasticity."],["dc.identifier.doi","10.3389/fncir.2013.00167"],["dc.identifier.fs","599562"],["dc.identifier.gro","3151828"],["dc.identifier.pmid","24155695"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8658"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","1662-5110"],["dc.relation.orgunit","Fakultät für Physik"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Action Potentials"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Hippocampus"],["dc.subject.mesh","Models, Neurological"],["dc.subject.mesh","Nerve Net"],["dc.subject.mesh","Neurons"],["dc.subject.mesh","Optogenetics"],["dc.subject.mesh","Rats"],["dc.subject.mesh","Rats, Wistar"],["dc.title","Optogenetic stimulation effectively enhances intrinsically generated network synchrony"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1078"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","1091"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Martin, Sabine"],["dc.contributor.author","Lazzarini, Marcio"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Balakrishnan, Saju"],["dc.contributor.author","Ninkovic, Milena"],["dc.contributor.author","El Hady, Ahmed"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Del Bel, Elaine"],["dc.contributor.author","Gomez, Felipe V."],["dc.date.accessioned","2018-10-08T06:24:14Z"],["dc.date.available","2018-10-08T06:24:14Z"],["dc.date.issued","2017"],["dc.description.abstract","The dysfunction of the small-conductance calcium-activated K+ channel SK3 has been described as one of the factors responsible for the progress of psychoneurological diseases, but the molecular basis of this is largely unknown. This report reveals through use of immunohistochemistry and computational tomography that long-term increased expression of the SK3 small-conductance calcium-activated potassium channel (SK3-T/T) in mice induces a notable bilateral reduction of the hippocampal area (more than 50 %). Histological analysis showed that SK3-T/T mice have cellular disarrangements and neuron discontinuities in the hippocampal formation CA1 and CA3 neuronal layer. SK3 overexpression resulted in cognitive loss as determined by the object recognition test. Electrophysiological examination of hippocampal slices revealed that SK3 channel overexpression induced deficiency of long-term potentiation in hippocampal microcircuits. In association with these results, there were changes at the mRNA levels of some genes involved in Alzheimer's disease and/or linked to schizophrenia, epilepsy, and autism. Taken together, these features suggest that augmenting the function of SK3 ion channel in mice may present a unique opportunity to investigate the neural basis of central nervous system dysfunctions associated with schizophrenia, Alzheimer's disease, or other neuropsychiatric/neurodegenerative disorders in this model system. As a more detailed understanding of the role of the SK3 channel in brain disorders is limited by the lack of specific SK3 antagonists and agonists, the results observed in this study are of significant interest; they suggest a new approach for the development of neuroprotective strategies in neuropsychiatric/neurodegenerative diseases with SK3 representing a potential drug target."],["dc.identifier.doi","10.1007/s12035-015-9680-6"],["dc.identifier.pmid","26803493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15872"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1559-1182"],["dc.title","SK3 Channel Overexpression in Mice Causes Hippocampal Shrinkage Associated with Cognitive Impairments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]