Czéh, Boldizsár

[["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","1025"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","1034"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Coe, Christopher L"],["dc.contributor.author","Kramer, Marian"],["dc.contributor.author","Czéh, Boldizsár"],["dc.contributor.author","Gould, Elizabeth"],["dc.contributor.author","Reeves, Alison J"],["dc.contributor.author","Kirschbaum, Clemens"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2022-10-06T13:33:38Z"],["dc.date.available","2022-10-06T13:33:38Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1016/S0006-3223(03)00698-X"],["dc.identifier.pii","S000632230300698X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115686"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0006-3223"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Prenatal stress diminishes neurogenesis in the dentate gyrus of juvenile Rhesus monkeys"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","290"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","293"],["dc.bibliographiccitation.volume","947"],["dc.contributor.author","Fischer, Anja K"],["dc.contributor.author","von Rosenstiel, Philipp"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Goula, Daniel"],["dc.contributor.author","Almeida, Osborne F.X"],["dc.contributor.author","Czéh, Boldizsár"],["dc.date.accessioned","2022-10-06T13:33:39Z"],["dc.date.available","2022-10-06T13:33:39Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1016/S0006-8993(02)03042-1"],["dc.identifier.pii","S0006899302030421"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115691"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0006-8993"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","The prototypic mineralocorticoid receptor agonist aldosterone influences neurogenesis in the dentate gyrus of the adrenalectomized rat"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","43"],["dc.bibliographiccitation.issue","1-3"],["dc.bibliographiccitation.journal","European Journal of Pharmacology"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","598"],["dc.contributor.author","Michael-Titus, Adina T."],["dc.contributor.author","Albert, Monika"],["dc.contributor.author","Michael, Gregory J."],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Pudovkina, Olga"],["dc.contributor.author","van der Hart, Marieke G.C."],["dc.contributor.author","Hesselink, Mayke B."],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Czéh, Boldizsár"],["dc.date.accessioned","2022-10-06T13:33:06Z"],["dc.date.available","2022-10-06T13:33:06Z"],["dc.date.issued","2008"],["dc.identifier.doi","10.1016/j.ejphar.2008.09.006"],["dc.identifier.pii","S0014299908009436"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115546"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0014-2999"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","SONU20176289, a compound combining partial dopamine D2 receptor agonism with specific serotonin reuptake inhibitor activity, affects neuroplasticity in an animal model for depression"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","369"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.lastpage","374"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Schmelting, Barthel"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:30:14Z"],["dc.date.available","2018-11-07T09:30:14Z"],["dc.date.issued","2006"],["dc.description.abstract","Pathomorphological studies described pathological heterogeneity in patients with multiple sclerosis (MS). Different effector mechanisms might therefore be responsible for lesion formation in MS. The present report shows that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in common marmoset monkeys reflects one specific lesional subtype of MS, namely MS pattern 11 lesions with antibody/complement-mediated damage. MOG-induced EAE in marmoset monkeys will, therefore, provide an ideal model for therapeutic approaches directed against B-cell/antibody/complement in MS."],["dc.identifier.doi","10.1191/1352458506ms1290oa"],["dc.identifier.isi","000239431200002"],["dc.identifier.pmid","16900750"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31257"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1352-4585"],["dc.title","Myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in the common marmoset reflects the immunopathology of pattern II multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","161"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","166"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Lucassen, Paul J."],["dc.contributor.author","Vollmann-Honsdorf, Gesa K."],["dc.contributor.author","Gleisberg, Mira"],["dc.contributor.author","Czéh, Boldizsár"],["dc.contributor.author","De Kloet, E. Ron"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2022-10-06T13:34:22Z"],["dc.date.available","2022-10-06T13:34:22Z"],["dc.date.issued","2001"],["dc.identifier.doi","10.1046/j.0953-816x.2001.01629.x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115894"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.issn","0953-816X"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Chronic psychosocial stress differentially affects apoptosis in hippocampal subregions and cortex of the adult tree shrew"],["dc.title.alternative","Apoptosis in the tree shrew hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","548"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","557"],["dc.bibliographiccitation.volume","180"],["dc.contributor.author","Czéh, Boldizsár"],["dc.contributor.author","Pudovkina, Olga"],["dc.contributor.author","van der Hart, Marieke G. C."],["dc.contributor.author","Simon, Mária"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2022-10-06T13:27:11Z"],["dc.date.available","2022-10-06T13:27:11Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1007/s00213-005-2184-8"],["dc.identifier.pii","2184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115273"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1432-2072"],["dc.relation.issn","0033-3158"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Examining SLV-323, a novel NK1 receptor antagonist, in a chronic psychosocial stress model for depression"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","190"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Perez-Cruz, Claudia"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Fluegge, Gabriele"],["dc.date.accessioned","2018-11-07T11:13:53Z"],["dc.date.available","2018-11-07T11:13:53Z"],["dc.date.issued","2008"],["dc.description.abstract","The prefrontal cortex (PFC) is implicated in a number of higher cognitive functions as well as processing emotions and regulation of stress responses. Hemispheric specialization of the PFC in humans in emotional processing is well documented, and there is evidence that a similar functional lateralization is present in all mammals. Recent findings suggest the possibility of an intrinsic structural hemispheric asymmetry in the rat medial PFC (mPFC). Specifically, interhemispheric differences have been found in the architecture of pyramidal cell apical dendritic trees together with hemispheric asymmetry in cell proliferation including gliogenesis. It is now well established that chronic stress has a profound impact on neural plasticity in a number of corticolimbic structures and affects the etiology, pathophysiology, and therapeutic outcome of most psychiatric disorders. We summarize recent experimental data documenting pronounced dendritic remodeling of pyramidal cells and suppressed gliogenesis in the mPFC of rats subjected to chronic stress or to artificially elevated glucocorticoid levels. The stress affect on these structural elements seems to be hemispheric specific, often abolishing or even reversing natural asymmetries seen at the cellular level. We discuss these preclinical observations with respect to clinical findings that show impaired function, altered lateralization and histopathological changes in the PFC in psychiatric patients. We argue that it is important to define the kinds of structural changes that result from long-term stress exposure because this knowledge will improve the identification of cellular endophenotypes in various psychiatric disorders. (c) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.bbr.2008.02.031"],["dc.identifier.isi","000255766800001"],["dc.identifier.pmid","18384891"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54000"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0166-4328"],["dc.title","Chronic stress-induced cellular changes in the medial prefrontal cortex and their potential clinical implications: Does hemisphere location matter?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","250"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","260"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Lucassen, Paul J."],["dc.date.accessioned","2018-11-07T10:59:52Z"],["dc.date.available","2018-11-07T10:59:52Z"],["dc.date.issued","2007"],["dc.description.abstract","Even though in vivo imaging studies document significant reductions of hippocampal volume in depressed patients, the exact underlying cellular mechanisms are unclear. Since stressful life events are associated with an increased risk of developing depression, preclinical studies in which animals are exposed to chronic stress have been used to understand the hippocampal shrinkage in depressed patients. Based on morphometrical studies in these models, parameters like dendritic retraction, suppressed adult neurogenesis and neuronal death, all due to elevated levels of glucocorticoids, have been suggested as major causative factors in hippocampal shrinkage. However, histopathological studies examining hippocampi of depressed individuals have so far failed to confirm either a massive neuronal loss or a suppression of dentate neurogenesis, an event that is notably very rare in adult or elderly humans. In fact, many of the structural changes and the volume reduction appear to be reversible. Clearly, more histopathological studies are needed; especially ones that (a) employ stereological quantification, (b) focus on specific cellular elements and populations, and (c) are performed in nonmedicated depressed patients. We conclude that mainly other factors, like alterations in the somatodendritic, axonal, and synaptic components and putative glial changes are most likely to explain the hippocampal shrinkage in depression, while shifts in fluid balance or changes in the extracellular space cannot be excluded either."],["dc.identifier.doi","10.1007/s00406-007-0728-0"],["dc.identifier.isi","000248941200002"],["dc.identifier.pmid","17401728"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50798"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0940-1334"],["dc.title","What causes the hippocampal volume decrease in depression?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1146"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","British Journal of Pharmacology"],["dc.bibliographiccitation.lastpage","1186"],["dc.bibliographiccitation.volume","179"],["dc.contributor.author","Borbély, Éva"],["dc.contributor.author","Simon, Mária"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Wiborg, Ove"],["dc.contributor.author","Czéh, Boldizsár"],["dc.contributor.author","Helyes, Zsuzsanna"],["dc.date.accessioned","2022-10-06T13:24:59Z"],["dc.date.available","2022-10-06T13:24:59Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1111/bph.15753"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114722"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1476-5381"],["dc.relation.issn","0007-1188"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Novel drug developmental strategies for treatment‐resistant depression"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]