Wojcik, Sonja M.

[["dc.bibliographiccitation.artnumber","27"],["dc.bibliographiccitation.journal","BMC Biology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Agarwal, Amit"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Wojcik, Sonja M."],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2011"],["dc.description.abstract","BACKGROUND: Erythropoietin (EPO) and its receptor (EPOR) are expressed in the developing brain and their transcription is upregulated in adult neurons and glia upon injury or neurodegeneration. We have shown neuroprotective effects and improved cognition in patients with neuropsychiatric diseases treated with EPO. However, the critical EPO targets in brain are unknown, and separation of direct and indirect effects has remained difficult, given the role of EPO in hematopoiesis and brain oxygen supply. RESULTS: Here we demonstrate that mice with transgenic expression of a constitutively active EPOR isoform (cEPOR) in pyramidal neurons of cortex and hippocampus exhibit enhancement of spatial learning, cognitive flexibility, social memory, and attentional capacities, accompanied by increased impulsivity. Superior cognitive performance is associated with augmented long-term potentiation of cEPOR expressing neurons in hippocampal slices. CONCLUSIONS: Active EPOR stimulates neuronal plasticity independent of any hematopoietic effects and in addition to its neuroprotective actions. This property of EPOR signaling should be exploited for defining novel strategies to therapeutically enhance cognitive performance in disease conditions."],["dc.format.extent","16"],["dc.identifier.doi","10.1186/1741-7007-9-27"],["dc.identifier.gro","3150548"],["dc.identifier.pmid","21527022"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6376"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7322"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Expression of constitutively active erythropoietin receptor in pyramidal neurons of cortex and hippocampus boosts higher cognitive functions in mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Brain Structure and Function"],["dc.bibliographiccitation.lastpage","26"],["dc.contributor.author","Rahman, Jamilur"],["dc.contributor.author","Besser, Stefanie"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Eulenburg, Volker"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Wojcik, Sonja M."],["dc.contributor.author","Hülsmann, Swen"],["dc.date.accessioned","2019-07-09T11:41:21Z"],["dc.date.available","2019-07-09T11:41:21Z"],["dc.date.issued","2014"],["dc.description.abstract","Both glycinergic and GABAergic neurons require the vesicular inhibitory amino acid transporter (VIAAT) for synaptic vesicle filling. Presynaptic GABA concentrations are determined by the GABA synthesizing enzymes glutamate decarboxylase (GAD)65 and GAD67, whereas the presynaptic glycine content depends on the plasma membrane glycine transporter 2 (GlyT2). Although severely impaired, glycinergic transmission is not completely absent in GlyT2-knockout mice, suggesting that other routes of glycine uptake or de novo synthesis of glycine exist in presynaptic terminals. To investigate the consequences of a complete loss of glycinergic transmission, we generated a mouse line with a conditional ablation of VIAAT in glycinergic neurons by crossing mice with loxP-flanked VIAAT alleles with a GlyT2-Cre transgenic mouse line. Interestingly, conditional VIAAT knockout (VIAAT cKO) mice were not viable at birth. In addition to the dominant respiratory failure, VIAAT cKO showed an umbilical hernia and a cleft palate. Immunohistochemistry revealed an almost complete depletion of VIAAT in the brainstem. Electrophysiology revealed the absence of both spontaneous glycinergic and GABAergic inhibitory postsynaptic currents (IPSCs) from hypoglossal motoneurons. Our results demonstrate that the deletion of VIAAT in GlyT2-Cre expressing neurons also strongly affects GABAergic transmission and suggest a large overlap of the glycinergic and the GABAergic neuron population during early development in the caudal parts of the brain."],["dc.identifier.doi","10.1007/s00429-014-0829-2"],["dc.identifier.pmid","25027639"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11988"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58409"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Genetic ablation of VIAAT in glycinergic neurons causes a severe respiratory phenotype and perinatal death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","submitted_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Marx, Grit"],["dc.contributor.author","Besser, Stefanie"],["dc.contributor.author","Sicker, Marit"],["dc.contributor.author","Köhler, Susanne"],["dc.contributor.author","Hirrlinger, Petra G."],["dc.contributor.author","Wojcik, Sonja M."],["dc.contributor.author","Eulenburg, Volker"],["dc.contributor.author","Winkler, Ulrike"],["dc.contributor.author","Hülsmann, Swen"],["dc.date.accessioned","2020-12-10T18:44:31Z"],["dc.date.available","2020-12-10T18:44:31Z"],["dc.date.issued","2019"],["dc.description.abstract","Inhibitory neurons crucially contribute to shaping the breathing rhythm in the brain stem. These neurons use GABA or glycine as neurotransmitter; or co-release GABA and glycine. However, the developmental relationship between GABAergic, glycinergic and cotransmitting neurons, and the functional relevance of cotransmitting neurons has remained enigmatic. Transgenic mice expressing fluorescent markers or the split-Cre system in inhibitory neurons were developed to track the three different interneuron phenotypes. During late embryonic development, the majority of inhibitory neurons in the ventrolateral medulla are cotransmitting cells, most of which differentiate into GABAergic and glycinergic neurons around birth and around postnatal day 4, respectively. Functional inactivation of cotransmitting neurons revealed an increase of the number of respiratory pauses, the cycle-by-cycle variability, and the overall variability of breathing. In summary, the majority of cotransmitting neurons differentiate into GABAergic or glycinergic neurons within the first 2 weeks after birth and these neurons contribute to fine-tuning of the breathing pattern."],["dc.identifier.doi","10.3389/fncel.2019.00517"],["dc.identifier.eissn","1662-5102"],["dc.identifier.pmid","31803026"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78488"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5102"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","GABA-Glycine Cotransmitting Neurons in the Ventrolateral Medulla: Development and Functional Relevance for Breathing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]