Flügge, Gabriele

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Psychoneuroendocrinology"],["dc.bibliographiccitation.lastpage","51"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Flügge, Gabriele"],["dc.date.accessioned","2022-10-06T13:32:51Z"],["dc.date.available","2022-10-06T13:32:51Z"],["dc.date.issued","1995"],["dc.identifier.doi","10.1016/0306-4530(94)E0006-U"],["dc.identifier.pii","0306453094E0006U"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115473"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0306-4530"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Modulation of binding sites for corticotropin-releasing hormone by chronic psychosocial stress"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","557"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Psychoneuroendocrinology"],["dc.bibliographiccitation.lastpage","565"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Johren, O."],["dc.contributor.author","Flugge, G."],["dc.date.accessioned","2022-10-06T13:32:51Z"],["dc.date.available","2022-10-06T13:32:51Z"],["dc.date.issued","1993"],["dc.identifier.doi","10.1016/0306-4530(93)90033-H"],["dc.identifier.pii","030645309390033H"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115472"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0306-4530"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Psychosocial conflict in the tree shrew: Effects on sympathoadrenal activity and blood pressure"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","187"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Flügge, G"],["dc.date.accessioned","2022-10-06T13:32:51Z"],["dc.date.available","2022-10-06T13:32:51Z"],["dc.date.issued","1996"],["dc.identifier.doi","10.1016/0306-4522(96)00292-8"],["dc.identifier.pii","0306452296002928"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115471"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0306-4522"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Alterations in the central nervous α2-adrenoceptor system under chronic psychosocial stress"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","417"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Physiology & Behavior"],["dc.bibliographiccitation.lastpage","427"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Flügge, Gabriele"],["dc.date.accessioned","2022-10-06T13:33:43Z"],["dc.date.available","2022-10-06T13:33:43Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1016/S0031-9384(03)00161-6"],["dc.identifier.pii","S0031938403001616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115712"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0031-9384"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Chronic social stress: effects on limbic brain structures"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Rygula, Rafal"],["dc.contributor.author","Flugge, G."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hiemke, Christoph"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.date.accessioned","2018-11-07T10:48:30Z"],["dc.date.available","2018-11-07T10:48:30Z"],["dc.date.issued","2004"],["dc.format.extent","S458"],["dc.identifier.isi","000224663002518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48208"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.publisher.place","New york"],["dc.relation.conference","24th CINP Congress"],["dc.relation.eventlocation","Paris, FRANCE"],["dc.relation.issn","1461-1457"],["dc.title","Chronic psychosocial stress in rats as a model of depression - Behavioral and pharmacological studies"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","53"],["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Araya Callis, Carolina"],["dc.contributor.author","Flügge, Gabriele"],["dc.contributor.author","Hülsmann, Swen"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:22:20Z"],["dc.date.available","2018-09-28T10:22:20Z"],["dc.date.issued","2012"],["dc.description.abstract","Chronic stress affects neuronal networks by inducing dendritic retraction, modifying neuronal excitability and plasticity, and modulating glial cells. To elucidate the functional consequences of chronic stress for the hippocampal network, we submitted adult rats to daily restraint stress for 3 weeks (6 h/day). In acute hippocampal tissue slices of stressed rats, basal synaptic function and short-term plasticity at Schaffer collateral/CA1 neuron synapses were unchanged while long-term potentiation was markedly impaired. The spatiotemporal propagation pattern of hypoxia-induced spreading depression episodes was indistinguishable among control and stress slices. However, the duration of the extracellular direct current potential shift was shortened after stress. Moreover, K(+) fluxes early during hypoxia were more intense, and the postsynaptic recoveries of interstitial K(+) levels and synaptic function were slower. Morphometric analysis of immunohistochemically stained sections suggested hippocampal shrinkage in stressed rats, and the number of cells that are immunoreactive for glial fibrillary acidic protein was increased in the CA1 subfield indicating activation of astrocytes. Western blots showed a marked downregulation of the inwardly rectifying K(+) channel Kir4.1 in stressed rats. Yet, resting membrane potentials, input resistance, and K(+)-induced inward currents in CA1 astrocytes were indistinguishable from controls. These data indicate an intensified interstitial K(+) accumulation during hypoxia in the hippocampus of chronically stressed rats which seems to arise from a reduced interstitial volume fraction rather than impaired glial K(+) buffering. One may speculate that chronic stress aggravates hypoxia-induced pathophysiological processes in the hippocampal network and that this has implications for the ischemic brain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.3389/fphar.2012.00053"],["dc.identifier.pmid","22470344"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7501"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15856"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1663-9812"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Restraint Stress Intensifies Interstitial K(+) Accumulation during Severe Hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","374"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain Research Bulletin"],["dc.bibliographiccitation.lastpage","379"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Hu, Wen"],["dc.contributor.author","Zhang, M."],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Zhang, W."],["dc.contributor.author","Fluegge, Gabriele"],["dc.date.accessioned","2018-11-07T08:54:17Z"],["dc.date.available","2018-11-07T08:54:17Z"],["dc.date.issued","2011"],["dc.description.abstract","Chronic stress, a risk factor for the development of psychiatric disorders, is known to induce alterations in neuronal networks in many brain areas. Previous studies have shown that chronic stress changes the expression of the cannabinoid receptor 1 (CB1) in the brains of adult rats, but neurophysiological consequences of these changes remained unclear. Here we demonstrate that chronic restraint stress causes a dysfunction in CBI mediated modulation of GABAergic transmission in the hippocampus. Using an established protocol, adult male Sprague Dawley rats were daily restrained for 21 days and whole-cell voltage clamp was performed at CA1 pyramidal neurons. When recording carbachol-evoked inhibitory postsynaptic currents (IPSCs) which presumably originate from CBI expressing cholecystokinin (CCK) interneurons, we found that depolarization-induced suppression of inhibition (DSI) was impaired by the stress. DSI is a form of short-term plasticity at GABAergic synapses that is known to be CB1 mediated and has been suggested to be involved in hippocampal information encoding. Chronic stress attenuated the depolarization-induced suppression of the frequency of carbachol-evoked IPSCs. Incubation with a CBI receptor antagonist prevented this DSI effect in control but not in chronically stressed animals. The stress-induced impairment of CB1-mediated short-term plasticity at GABAergic synapses may underlie cognitive deficits which are commonly observed in animal models of stress as well as in patients with stress-related psychiatric disorders. (C) 2011 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; Ministry of Lower Saxony, Germany"],["dc.identifier.doi","10.1016/j.brainresbull.2011.04.005"],["dc.identifier.isi","000293719700009"],["dc.identifier.pmid","21527320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22636"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0361-9230"],["dc.title","Chronic restraint stress impairs endocannabinoid mediated suppression of GABAergic signaling in the hippocampus of adult male rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","247"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Pharmacology Biochemistry and Behavior"],["dc.bibliographiccitation.lastpage","258"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Flügge, Gabriele"],["dc.date.accessioned","2022-10-06T13:33:46Z"],["dc.date.available","2022-10-06T13:33:46Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1016/S0091-3057(02)00795-5"],["dc.identifier.pii","S0091305702007955"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115722"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0091-3057"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Social stress in tree shrews"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e431"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Boeer, Ulrike"],["dc.contributor.author","Alejel, Tahseen"],["dc.contributor.author","Beimesche, Stephan"],["dc.contributor.author","Cierny, Irmgard"],["dc.contributor.author","Krause, Doris"],["dc.contributor.author","Knepel, Willhart"],["dc.contributor.author","Fluegge, Gabriele"],["dc.date.accessioned","2018-11-07T11:02:26Z"],["dc.date.available","2018-11-07T11:02:26Z"],["dc.date.issued","2007"],["dc.description.abstract","Background. It has been suggested that stress provokes neuropathological changes and may thus contribute to the precipitation of affective disorders such as depression. Likewise, the pharmacological therapy of depression requires chronic treatment and is thought to induce a positive neuronal adaptation, presumably based on changes in gene transcription. The transcription factor cAMP-responsive element binding protein (CREB) and its binding site (CRE) have been suggested to play a major role in both the development of depression and antidepressive therapy. Methodology/Principle Findings. To investigate the impact of stress and antidepressant treatment on CRE/CREB transcriptional activity, we generated a transgenic mouse line in which expression of the luciferase reporter gene is controlled by four copies of CRE. In this transgene, luciferase enzyme activity and protein were detected throughout the brain, e. g., in the hippocampal formation. Chronic social stress significantly increased (by 45 to 120%) CRE/CREB-driven gene expression measured as luciferase activity in several brain regions. This was also reflected by increased CREB-phosphorylation determined by immunoblotting. Treatment of the stressed mice with the antidepressant imipramine normalized luciferase expression to control levels in all brain regions and likewise reduced CREB-phosphorylation. In non-stressed animals, chronic (21 d) but not acute (24 h) treatment with imipramine (2 x 10 mg/kg/d) reduced luciferase expression in the hippocampus by 40-50%. Conclusions/Significance. Our results emphasize a role of CREB in stress-regulated gene expression and support the view that the therapeutic actions of antidepressants are mediated via CRE/CREB-directed transcription."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [SFB 402 (A3)]"],["dc.identifier.doi","10.1371/journal.pone.0000431"],["dc.identifier.isi","000207445800013"],["dc.identifier.pmid","17487276"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8241"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51383"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","CRE/CREB-Driven Up-Regulation of Gene Expression by Chronic Social Stress in CRE-Luciferase Transgenic Mice: Reversal by Antidepressant Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","1197"],["dc.contributor.author","Cooper, Ben"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Flügge, Gabriele"],["dc.date.accessioned","2022-10-06T13:33:00Z"],["dc.date.available","2022-10-06T13:33:00Z"],["dc.date.issued","2008"],["dc.identifier.doi","10.1016/j.brainres.2007.11.066"],["dc.identifier.pii","S0006899307028429"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115519"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0006-8993"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Glycoprotein M6a is present in glutamatergic axons in adult rat forebrain and cerebellum"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]