Stefanie Tinnes
University of Freiburg
6 Papers
42 Citations
Stefanie Tinnes is an academic researcher from University of Freiburg. The author has contributed to research in topics: Dentate gyrus & Reelin. The author has an hindex of 6, co-authored 6 publications. Previous affiliations of Stefanie Tinnes include University Medical Center Freiburg.
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Papers
Exogenous reelin prevents granule cell dispersion in experimental epilepsy.
Martin C. Müller,Matthias Osswald,Stefanie Tinnes,Ute Häussler,Anne Jacobi,Eckart Förster,Michael Frotscher,Carola A. Haas +7 more
TL;DR: The findings highlight the crucial role of reelin for the maintenance of granule cell lamination in the dentate gyrus of adult mice and show that a reelin deficiency is causally involved in GCD development.
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Early life stress stimulates hippocampal reelin gene expression in a sex-specific manner: evidence for corticosterone-mediated action.
Claus M. Gross,Armin Flubacher,Stefanie Tinnes,Andrea Heyer,Marie Scheller,Inga Herpfer,Mathias Berger,Michael Frotscher,Klaus Lieb,Klaus Lieb,Carola A. Haas +10 more
TL;DR: Results show a sex‐specific regulation of reelin gene expression by early life experience, most likely mediated by corticosterone.
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Regulation of action potential delays via voltage-gated potassium Kv1.1 channels in dentate granule cells during hippocampal epilepsy.
Florian Kirchheim,Florian Kirchheim,Stefanie Tinnes,Carola A. Haas,Michael Stegen,Michael Stegen,Jakob Wolfart,Jakob Wolfart +7 more
TL;DR: The AP timing of DG cells is effectively controlled via scaling of Kv1.1 subunit transcription and, with this antiepileptic mechanism, DG cells delay their responses during hyperexcitation.
Epilepsy-Induced Motility of Differentiated Neurons
Xuejun Chai,Gert Münzner,Shanting Zhao,Stefanie Tinnes,Janina Kowalski,Ute Häussler,Christina Young,Carola A. Haas,Michael Frotscher +8 more
TL;DR: It is shown that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD, and is suggested that KA-induced motility of differentiatedGCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptic activity.
TIMP-1 inhibits the proteolytic processing of Reelin in experimental epilepsy
TL;DR: Evidence is presented that epileptic conditions inhibit MMP activity by up‐regulation of endogenous TIMP‐1, which in turn leads to extracellular accumulation of uncleaved and inactive Reelin and thereby to GCD, similar to that observed after KA treatment.
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