Hülsmann, Swen

[["dc.bibliographiccitation.firstpage","342"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","352"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Latal, A. Tobias"],["dc.contributor.author","Kremer, Thomas"],["dc.contributor.author","Gomeza, Jesus"],["dc.contributor.author","Eulenburg, Volker"],["dc.contributor.author","Huelsmann, Swen"],["dc.date.accessioned","2018-11-07T08:40:59Z"],["dc.date.available","2018-11-07T08:40:59Z"],["dc.date.issued","2010"],["dc.description.abstract","Mice deficient for the neuronal glycine transporter subtype 2 (GlyT2) die during the second postnatal week after developing neuromotor deficiencies, which resembles severe forms of human hyperekplexia. This phenotype has been attributed to a dramatic reduction in glycinergic neurotransmission. In the present study we analyzed the development of GABAergic and glycinergic synaptic transmission in GlyT2-knockout mice during early postnatal life. Anti-glycine immunohistochemistry in spinal cord and brainstem slices and whole-cell voltage-clamp recordings of glycinergic inhibitory postsynaptic currents (IPSCs) from hypoglossal motoneurons revealed strikingly reduced levels of synaptic glycine already at birth. Since GABA and glycine use the same vesicular inhibitory amino acid transporter (VIAAT or VGAT) we also analysed GABAergic neurotransmission. No increase of GABA immunoreactivity was observed in the spinal cord and brainstem of GlyT2(-/-) mice at any stage of postnatal development. Correspondingly no up-regulation of GABAergic IPSCs was detected in GlyT2(-/-) hypoglossal motoneurons. These data suggest that in the first postnatal week, loss of the glycine transporter 2 is neither compensated by glycine de-novo synthesis nor by up-regulation of the GABAergic transmission in GlyT2(-/-) mice. (C) 2010 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.mcn.2010.04.005"],["dc.identifier.isi","000279525600004"],["dc.identifier.pmid","20447457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19369"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1044-7431"],["dc.title","Development of synaptic inhibition in glycine transporter 2 deficient mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3888"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.lastpage","3899"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Papadopoulos, Theofilos"],["dc.contributor.author","Korte, Martin"],["dc.contributor.author","Eulenburg, Volker"],["dc.contributor.author","Kubota, Hisahiko"],["dc.contributor.author","Retiounskaia, Marina"],["dc.contributor.author","Harvey, Robert J."],["dc.contributor.author","Harvey, Kirsten"],["dc.contributor.author","O'Sullivan, Gregory A."],["dc.contributor.author","Laube, Bodo"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Geiger, Joerg R. P."],["dc.contributor.author","Betz, Heinrich"],["dc.date.accessioned","2018-11-07T10:58:38Z"],["dc.date.available","2018-11-07T10:58:38Z"],["dc.date.issued","2007"],["dc.description.abstract","Collybistin (Cb) is a brain-specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb-deficient mice display a region-specific loss of postsynaptic gephyrin and GABA(A) receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long-term potentiation is enhanced, and long-term depression reduced, in Cb-deficient hippocampal slices. Consistent with the anatomical and electro-physiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin-dependent clustering of a specific set of GABA(A) receptors, but not required for glycine receptor postsynaptic localization."],["dc.description.sponsorship","Medical Research Council [G0601585, G0501258]"],["dc.identifier.doi","10.1038/sj.emboj.7601819"],["dc.identifier.isi","000249691800002"],["dc.identifier.pmid","17690689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50510"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0261-4189"],["dc.title","Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin-deficient mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]