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","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","738"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","747"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Perez-Cruz, Claudia"],["dc.contributor.author","Simon, Maria"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Fluegge, Gabriele"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2018-11-07T08:33:00Z"],["dc.date.available","2018-11-07T08:33:00Z"],["dc.date.issued","2009"],["dc.description.abstract","Pyramidal neurons of the rat medial prefrontal cortex have been shown to react to chronic stress by retracting their apical dendrites and by spine loss. We extended these findings by focusing on the basilar dendritic tree of layer III pyramidal neurons in both hemispheres of the rat prelimbic cortex. Animals were subjected to daily restraint stress for 1 week (6 h/day), during either the resting or the activity period. The morphology of basilar dendrites and spines of Golgi-Cox-stained neurons in the left and right hemispheres was digitally reconstructed and analyzed. We observed the following: (i) there was an inherent hemispheric asymmetry in control rats during the resting period: the number of spines on proximal dendrites was higher in the left than in the right hemisphere; (ii) basal dendrites in controls displayed a diurnal variation: there was more dendritic material during the resting period than in the activity period; (iii) chronic stress reduced the length of basal dendrites in only the right prelimbic cortex; (iv) chronic stress reduced spine density on proximal basal dendrites; (v) restraint stress during the activity period had more pronounced effects on the physiological stress parameters than restraint stress during the resting period. Our results show dynamic hemisphere-dependent structural changes in pyramidal neurons of the rat prelimbic cortex that are tightly linked to periods of resting and activity. These morphological alterations reflect the capacity of the neurons to react to external stimuli and mirror presumptive changes in neuronal communication."],["dc.identifier.doi","10.1111/j.1460-9568.2009.06622.x"],["dc.identifier.isi","000263451700008"],["dc.identifier.pmid","19200065"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17466"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0953-816X"],["dc.title","Hemispheric differences in basilar dendrites and spines of pyramidal neurons in the rat prelimbic cortex: activity- and stress-induced changes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1693"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","1707"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Hu, Wen"],["dc.contributor.author","Zhang, M."],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Fluegge, Gabriele"],["dc.contributor.author","Zhang, W."],["dc.date.accessioned","2018-11-07T08:41:57Z"],["dc.date.available","2018-11-07T08:41:57Z"],["dc.date.issued","2010"],["dc.description.abstract","Stress facilitates the development of psychiatric disorders in vulnerable individuals. It affects physiological functions of hippocampal excitatory neurons, but little is known about the impact of stress on the GABAergic network. Here, we studied the effects of stress and a synthetic glucocorticoid on hippocampal GABAergic neurotransmission and network function focusing on two perisomatic interneurons, the parvalbumin (PV)- and the cholecystokinin (CCK)-positive neurons. In acute hippocampal slices of rat, application of the potent glucocorticoid receptor (GR) agonist dexamethasone (DEX) caused a rapid increase in spontaneous inhibitory postsynaptic currents (sIPSCs) in CA1 pyramidal neurons. This effect was mediated by a nongenomic GR that evoked nitric oxide (NO) release from pyramidal neurons. Retrograde NO signaling caused the augmentation of GABA release from the interneurons and increased CCK release, which in turn further enhanced the activity of the PV-positive cells. Interestingly, chronic restraint stress also resulted in increased sIPSCs in CA1 pyramidal neurons that were Ca(2+)-dependent and an additional DEX application elicited no further effect. Concomitantly, chronic stress reduced the number of PV-immunoreactive cells and impaired rhythmic sIPSCs originating from the PV-positive neurons. In contrast, the CCK-positive neurons remained unaffected. We therefore propose that, in addition to the immediate effect, the sustained activation of nongenomic GRs during chronic stress injures the PV neuron network and results in an imbalance in perisomatic inhibition mediated by the PV and CCK interneurons. This stress-induced dysfunctional inhibitory network may in turn impair rhythmic oscillations and thus lead to cognitive deficits that are common in stress-related psychiatric disorders. Neuropsychopharmacology (2010) 35, 1693-1707; doi:10.1038/npp.2010.31; published online 31 March 2010"],["dc.identifier.doi","10.1038/npp.2010.31"],["dc.identifier.isi","000278730300009"],["dc.identifier.pmid","20357756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19584"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0893-133X"],["dc.title","Stress Impairs GABAergic Network Function in the Hippocampus by Activating Nongenomic Glucocorticoid Receptors and Affecting the Integrity of the Parvalbumin-Expressing Neuronal Network"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1249"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Current Drug Targets"],["dc.bibliographiccitation.lastpage","1261"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Fluegge, Gabriele"],["dc.date.accessioned","2018-11-07T09:19:32Z"],["dc.date.available","2018-11-07T09:19:32Z"],["dc.date.issued","2013"],["dc.description.abstract","Numerous clinical evidences support the notion that glial changes in fronto-limbic brain areas could contribute to the pathophysiology of mood disorders. Glial alterations have been reported not only in patients, but also in various kinds of animal models for depression. Molecular and cellular data suggest that all the major classes of glial cells are affected in these conditions, including astrocytes, oligodendrocytes, NG2-positive cells and microglia. The aim of this review was to summarize the currently available experimental results demonstrating alterations in glial morphology and functioning in animal models for mood disorders. Better understanding of these glial changes affecting neuronal activity could help us to identify novel targets for the development of antidepressant drugs."],["dc.identifier.isi","000324805500005"],["dc.identifier.pmid","23597041"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28663"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bentham Science Publ Ltd"],["dc.relation.issn","1873-5592"],["dc.relation.issn","1389-4501"],["dc.title","Altered Glial Plasticity in Animal Models for Mood Disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","315"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Behavioural Pharmacology"],["dc.bibliographiccitation.lastpage","325"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Flugge, G."],["dc.date.accessioned","2018-11-07T10:45:47Z"],["dc.date.available","2018-11-07T10:45:47Z"],["dc.date.issued","2004"],["dc.description.abstract","Despite decades of research on psychiatric disorders, the aetiology and precise biological mechanisms that underlie depressive diseases are still poorly understood. There is increasing evidence that psychiatric disorders not only have a neurochemical basis but are also associated with morphological alterations in central nervous neurons and/or glial cells. Antidepressants may act by restoring structure as well as function of neural networks, meaning that they may, as a fundamental principle, affect neural plasticity underlying normal brain functioning. To examine these novel concepts of the pathophysiology of depression and antidepressant medication we have carried out a series of experiments using the chronic psychosocial stress paradigm in male tree shrews, an animal model with a high validity for the pathophysiology of depressive disorders, in which the animals were treated with the tricyclic antidepressant compound clomipramine. We found that one month of stress reduced cell proliferation in the dentate gyrus, and decreased the total hippocampal volume. Gene transcription analysis revealed that, under these experimental conditions, expression of genes known to be involved in processes of cell differentiation is suppressed. These effects of social conflict on hippocampal cells, including gene transcription, and on the entire hippocampal volume could be counteracted by chronic treatment with the antidepressant clomipramine. Stress also induced a constant hyperactivity of the hypothalamic-pituitary-adrenal axis, and suppressed both motor and marking behaviour. These neuroendocrine and behavioural stress-induced changes were also re-normalized by clomipramine. (C) 2004 Lippincott Williams Wilkins."],["dc.identifier.doi","10.1097/00008877-200409000-00003"],["dc.identifier.isi","000223965700002"],["dc.identifier.pmid","15343055"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47586"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0955-8810"],["dc.title","Examining novel concepts of the pathophysiology of depression in the chronic psychosocial stress paradigm in tree shrews"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","982"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","992"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Herzog, C. J."],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Corbach, S."],["dc.contributor.author","Wuttke, Wolfgang"],["dc.contributor.author","Schulte-Herbrueggen, O."],["dc.contributor.author","Hellweg, R."],["dc.contributor.author","Fluegge, Gabriele"],["dc.contributor.author","Fuchs, E."],["dc.date.accessioned","2018-11-07T08:31:34Z"],["dc.date.available","2018-11-07T08:31:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Epidemiological studies demonstrate that affective disorders are at least twice as common in women as in men, but surprisingly, very few preclinical studies have been conducted on female experimental animals. Therefore, the necessity of developing valid animal models for studying the pathophysiology of stress-related disorders in women is obvious. Chronic social stress has the potential to induce depression in humans and therefore we characterize here a chronic social instability stress paradigm in female rats. This consists of a 4-week period with alternating stressful social situations, including phases of isolation and crowding, in an unpredictable manner. At the physiological level, increased adrenal weight and plasma corticosterone levels indicated hyperactivity of the hypothalamus-pituitary-ad renal axis. Elevated plasma luteinizing hormone and disruption of the estrus cycle together with increased serum prolactin levels revealed disrupted regulation of the hypothalamus-pituitary-gonadal axis. Body temperature regulation was affected during the last week of stress such that stressed rats reduced their body temperature less during the rest phase than the controls, thus exhibiting a flattened temperature curve. Behaviorally, chronically stressed rats showed reduced sucrose preference and food intake. However, we did not observe any effect of stress on performance in the forced swim test and hippocampal neurotrophin levels were similarly unaffected. Our results indicate that, by using this social instability paradigm, female rats can be kept under chronic stress for weeks without habituation, and that ultimately the animals develop a depressive-like phenotype. This model may provide a valuable tool for further analyses of the neurobiology of stress-related disorders in women and has the potential to serve as a paradigm for screening novel antidepressant drugs with special efficacy in women. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved."],["dc.description.sponsorship","Bettencourt-Schueller Fondation"],["dc.identifier.doi","10.1016/j.neuroscience.2009.01.059"],["dc.identifier.isi","000264715200007"],["dc.identifier.pmid","19356682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17150"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0306-4522"],["dc.title","CHRONIC SOCIAL INSTABILITY STRESS IN FEMALE RATS: A POTENTIAL ANIMAL MODEL FOR FEMALE DEPRESSION"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Roelleke, Ulrike"],["dc.contributor.author","Fluegge, Gabriele"],["dc.contributor.author","Plehm, Stephanie"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Uchanska-Ziegler, Barbara"],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Walter, Lutz"],["dc.date.accessioned","2018-11-07T09:37:05Z"],["dc.date.available","2018-11-07T09:37:05Z"],["dc.date.issued","2006"],["dc.description.abstract","It has been supposed that central nervous neurons do not express MHC class I molecules. However, recent studies clearly demonstrated functional MHC class I expression in the rodent brain. In the present study, we have extended these studies and investigated the presence of MHC class I transcripts and proteins in the brain of a non-human primate species, the common marmoset monkey (Callithrix jacchus). Using in-situ hybridization, we found strong expression of MHC class I transcripts in neocortex, hippocampal-formation, substantia nigra and nucleus ruber. In-situ hybridization with emulsion autoradiography demonstrated MHC class I mRNA in distinct pyramidal neurons of cortex and hippocampus, in granule neurons of the dentate gyrus, in dopaminergic neurons of substantia nigra and in motor neurons of nucleus ruber. Immunocytochemistry confirmed MHC class I protein expression in these neurons. Two monoclonal. antibodies, MRC-Ox18 and HB115, reacted differentially with MHC class I proteins on neuronal and non-neuronal cells, respectively. Interestingly, in marmoset monkeys that were immumosuppressed with FK506 (tacrolimus), expression of neuronal MHC class I proteins, which could be detected with MRC-Ox18, was either very low (neocortex, nucleus ruber, substantia nigra) or absent (hippocampus). In contrast, class I expression in endothelial cells, which was detected by HB115, was not affected by immunosuppression. Our data show that selected neurons in the brain of a non-human primate express MHC class I molecules and that this expression can be modulated by immunosuppression. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2006.04.015"],["dc.identifier.isi","000240323300006"],["dc.identifier.pmid","16750573"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32757"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Differential expression of major histocompatibility complex class I molecules in the brain of a New World monkey, the common marmoset (Callithrix jacchus)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","309"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Drug Development Research"],["dc.bibliographiccitation.lastpage","317"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Flugge, G."],["dc.date.accessioned","2018-11-07T10:57:02Z"],["dc.date.available","2018-11-07T10:57:02Z"],["dc.date.issued","2005"],["dc.description.abstract","Recent studies have provided evidence that mood disorders such as major depression not only have a neurochemical basis but are also associated with alterations in neuronal and glial Structures. Anti depressants may act by restoring structure as well as function of neural networks meaning that they may, as a fundamental principle, affect neural Plasticity underlying normal brain functioning. To examine this novel concept of the pathophysiology of depression and antidepressant medication, we have carried Out I series of experiments using the social stress paradigm in tree shrews, an animal model with a high validity for the pathophysiology of major depression. We found that 1 month of stress reduced the proliferation rate of newly born neurons in the dentate gyrus and decreased hippocampal volume. Notably, the suppressive effects of social conflict stress on hippocampal structure could be counteracted by treatments with different antidepressants such as clomipramine, tianeptine, and the selective NK1 receptor antagonists L-760735. In addition, the stress-induced decrease in number of parvalbumin-containing cells in the hippocampal formation, presumably GABAergic interneurons, was prevented by concomitant treatment with fluoxetine. These studies show that different classes of antidepressants can reverse the structural alterations of the hippocampal formation induced by stress."],["dc.identifier.doi","10.1002/ddr.20032"],["dc.identifier.isi","000234133400011"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50153"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0272-4391"],["dc.title","Preclinical approaches to examine novel concepts of the pathophysiology of depressive disorders: Lessons learned from tree shrews"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2746"],["dc.bibliographiccitation.journal","FRONTIERS IN BIOSCIENCE"],["dc.bibliographiccitation.lastpage","2758"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Flugge, G."],["dc.contributor.author","Czeh, Boldizsar"],["dc.date.accessioned","2018-11-07T09:18:58Z"],["dc.date.available","2018-11-07T09:18:58Z"],["dc.date.issued","2006"],["dc.description.abstract","Stress can be a threat to the physiological and psychological integrity of an individual and may result in psychic and behavioral changes. The stress response is mediated through in-concert activity of many brain areas and there is experimental evidence that stress induces structural changes in neuronal networks, in particular in the hippocampus, the prefrontal cortex and the amygdala. Within the hippocampal formation, stress exposure results in remodeling of dendrites of the CA3 pyramidal neurons and in reduced numbers of synapses on these neurons. Furthermore, stress inhibits adult neurogenesis in the dentate gyrus and appears to modulate the GABAergic system. In the prefrontal cortex, repeated exposure to stress causes dendritic retraction and loss of spines in pyramidal neurons whereas in the amygdala stress can elicit dendritic hypertrophy. These microscopically detectable changes in neuronal structures indicate the reorganization of neuronal networks. Moreover, molecular studies show that stress modulates expression of genes involved in neuronal differentiation and/or structural remodeling. Since a wealth of data documents the adverse effects of stress on emotions and cognition these alterations are commonly interpreted as the deleterious effect of chronic stress on the central nervous system. However, it is also possible that at least part of these changes reflect adaptive responses, as the network system rearranges its connections in order to cope with the changing requirements from the internal or external environment."],["dc.identifier.doi","10.2741/2004"],["dc.identifier.isi","000237382800063"],["dc.identifier.pmid","16720347"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28525"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers In Bioscience Inc"],["dc.relation.issn","1093-9946"],["dc.title","Remodeling of neuronal networks by stress"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]