Metzger, Friederike Luise

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Tectonics"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Zubovich, A."],["dc.contributor.author","Metzger, S."],["dc.contributor.author","Schöne, T."],["dc.contributor.author","Kley, J."],["dc.contributor.author","Mosienko, O."],["dc.contributor.author","Zech, C."],["dc.contributor.author","Moldobekov, B."],["dc.contributor.author","Shsarshebaev, A."],["dc.creator.author","A. Zubovich"],["dc.creator.author","S. Metzger"],["dc.creator.author","T. Schöne"],["dc.creator.author","J. Kley"],["dc.creator.author","O. Mosienko"],["dc.creator.author","C. Zech"],["dc.creator.author","B. Moldobekov"],["dc.creator.author","A. Sharshebaev"],["dc.date.accessioned","2022-12-06T14:42:55Z"],["dc.date.available","2022-12-06T14:42:55Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1029/2022TC007213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118449"],["dc.identifier.url","https://doi.org/10.1029/2022TC007213"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1944-9194"],["dc.relation.issn","0278-7407"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","Cyclic Fault Slip Under the Magnifier: Co‐ and Postseismic Response of the Pamir Front to the 2015 M w 7.2 Sarez, Central Pamir, Earthquake"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","84"],["dc.bibliographiccitation.journal","Journal of fluency disorders"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Neef, Nicole E."],["dc.contributor.author","Bütfering, Christoph"],["dc.contributor.author","Auer, Tibor"],["dc.contributor.author","Metzger, F. Luise"],["dc.contributor.author","Euler, Harald A."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Sommer, Martin"],["dc.date.accessioned","2018-10-09T11:33:47Z"],["dc.date.available","2018-10-09T11:33:47Z"],["dc.date.issued","2018"],["dc.description.abstract","Neuroimaging studies in persistent developmental stuttering repeatedly report altered basal ganglia functions. Together with thalamus and cerebellum, these structures mediate sensorimotor functions and thus represent a plausible link between stuttering and neuroanatomy. However, stuttering is a complex, multifactorial disorder. Besides sensorimotor functions, emotional and social-motivational factors constitute major aspects of the disorder. Here, we investigated cortical and subcortical gray matter regions to study whether persistent developmental stuttering is also linked to alterations of limbic structures."],["dc.identifier.doi","10.1016/j.jfludis.2017.04.002"],["dc.identifier.pmid","28595893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15903"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1873-801X"],["dc.title","Altered morphology of the nucleus accumbens in persistent developmental stuttering"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","50"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurophysiology"],["dc.bibliographiccitation.lastpage","59"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Metzger, F."],["dc.contributor.author","Kulik, A."],["dc.contributor.author","Sendtner, M."],["dc.contributor.author","Ballanyi, K."],["dc.date.accessioned","2018-11-07T11:09:56Z"],["dc.date.available","2018-11-07T11:09:56Z"],["dc.date.issued","2000"],["dc.description.abstract","Intracellular Ca2+ ([Ca2+](i)) was fluorometrically measured with fura-2 in lumbar motoneurons of acutely isolated spinal cord slices from embryonic rats. In ester-loaded cells, bath-applied glutamate (3 mu M to 1 mM) evoked a [Ca2+](i) increase by up to 250 nM that was abolished by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) plus 2-amino-5-phosphonovalerate (APV). CNQX or APV alone reduced the response by 82 and 25%, respectively. The glutamatergic agonists kainate (KA), quisqualate (QUI), and S-alpha-amino-3-hydroxy-5-methyl-4-isoxalone (S-AMPA) evoked a similar [Ca2+](i) transient as glutamate. N-methyl-D-aspartate (NMDA) was only effective to increase [Ca2+](i) in Mg2+-free saline, whereas [1S,3R]-1-aminocyclopentane-1,3-dicarboxylic acid([1S,3R]ACPD) had no effect. The glutamate-induced [Ca2+](i) rise was suppressed in Ca2+-free superfusate. Depletion of Ca2+ stores with cyclopiazonic acid (CPA) did not affect the response. Thirty-six percent of the [Ca2+](i) increase in response to membrane depolarization induced by a 50 mM K+ solution persisted on combined application of the voltage-gated Ca2+ channel blockers nifedipine, omega-conotoxin-GVIA and omega-agatoxin-IVA. In fura-2 dialyzed motoneurons, the glutamate-induced [Ca2+](i) increase was attenuated by similar to 70% after changing from current to voltage clamp. Forty percent of the remaining [Ca2+], transient and 20% of the concomitant inward current of 0.3 nA were blocked by Joro spider toxin-3 (JSTX). The results show that voltage-gated Ca2+ channels, including a major portion of R-type channels, constitute the predominant component of glutamate-induced [Ca2+](i) rises. NMDA and Ca2+-permeable KA/AMPA receptors contribute about equally to the remaining component of the Ca2+ rise. The results substantiate previous assumptions that Ca2+ influx through JSTX-sensitive KA/AMPA receptors is involved in (trophic) signaling in developing motoneurons."],["dc.identifier.isi","000084777800006"],["dc.identifier.pmid","10634852"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53108"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","0022-3077"],["dc.title","Contribution of Ca2+-permeable AMPA/KA receptors to glutamate-induced Ca2+ rise in embryonic lumbar motoneurons in situ"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]