Burkhardt, Susanne

[["dc.bibliographiccitation.firstpage","135"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","143"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Agbemenyah, Hope Yao"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Alzheimer's disease (AD) is the most common form of dementia in the elderly but effective therapeutic strategies to treat AD are not yet available. This is also due to the fact that the pathological mechanisms that drive the pathogenesis of sporadic AD are still not sufficiently understood and may differ on the individual level. Several risk factors such as altered insulin-like peptide (ILP) signaling have been linked to AD and modulating the ILP system has been discussed as a potential therapeutic avenue. Here we show that insulin-like growth factor binding protein 7 (IGFBP7), a protein that attenuates the function of ILPs, is up-regulated in the brains of AD patients and in a mouse model for AD via a process that involves altered DNA-methylation and coincides with decreased ILP signaling. Mimicking the AD-situation in wild type mice, by increasing hippocampal IGFBP7 levels leads to impaired memory consolidation. Consistently, inhibiting IGFBP7 function in mice that develop AD-like memory impairment reinstates associative learning behavior. These data suggest that IGFBP7 is a critical regulator of memory consolidation and might be used as a biomarker for AD. Targeting IGFBP7 could be a novel therapeutic avenue for the treatment of AD patients."],["dc.identifier.doi","10.1016/j.nbd.2013.09.011"],["dc.identifier.gro","3142193"],["dc.identifier.isi","000330553600013"],["dc.identifier.pmid","24075854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5566"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1095-953X"],["dc.relation.issn","0969-9961"],["dc.title","Insulin growth factor binding protein 7 is a novel target to treat dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2294"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Tan, Dun-Xian"],["dc.contributor.author","Manchester, Lucien C."],["dc.contributor.author","Burkhardt, S."],["dc.contributor.author","Sainz, Rosa M."],["dc.contributor.author","Mayo, J. C."],["dc.contributor.author","Kohen, R."],["dc.contributor.author","Shohami, E."],["dc.contributor.author","Huo, Y. S."],["dc.contributor.author","Hardeland, Ruediger"],["dc.contributor.author","Reiter, Russel J."],["dc.date.accessioned","2018-11-07T08:47:58Z"],["dc.date.available","2018-11-07T08:47:58Z"],["dc.date.issued","2001"],["dc.description.abstract","The biogenic amine N-1-acetyl-N-2-formyl-5-methoxykynuramine (AFMK) was investigated for its potential antioxidative capacity. AFMK is a metabolite generated through either an enzymatic or a chemical reaction pathway from melatonin. The physiological function of AFMK remains unknown. To our knowledge, this report is the first to document the potent antioxidant action of this biogenic amine. Cyclic voltammetry (CV) shows that AFMK donates two electrons at potentials of 456 mV and 668 mV, and therefore it functions as a reductive force. This function contrasts with all other physiological antioxidants that donate a single electron only when they neutralize free radicals. AFMK reduced 8-hydroxydeoxyguanosine formation induced by the incubation of DNA with oxidants significantly. Lipid peroxidation resulting from free radical damage to rat liver homogenates was also prevented by the addition of AFMK. The inhibitory effects of AFMK on both DNA and lipid damage appear to be dose-response related. In cell culture, AFMK efficiently reduced hippocampal neuronal death induced by either hydrogen peroxide, glutamate, or amyloid beta (25-35) peptide. AFMK is a naturally occurring molecule with potent free radical scavenging capacity (donating two electrons/molecule) and thus may be a valuable new antioxidant for preventing and treating free radical-related disorders."],["dc.identifier.isi","000170809900017"],["dc.identifier.pmid","11511530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21087"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.relation.issn","0892-6638"],["dc.title","N-1-acetyl-N-2-formyl-5-methoxykynuramine, a biogenic amine and melatonin metabolite, functions as a potent antioxidant"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Burkhardt, S."],["dc.contributor.author","Gruber, Eva"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.date.accessioned","2018-11-07T11:13:33Z"],["dc.date.available","2018-11-07T11:13:33Z"],["dc.date.issued","2008"],["dc.format.extent","271"],["dc.identifier.isi","000258855501400"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53922"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.publisher.place","New york"],["dc.relation.conference","26th Collegium Internationale Neuro-Psychopharmacologicum Congress (CINP)"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","1461-1457"],["dc.title","Common and disease-specific dysfunctions of brain systems underlying attentional and executive control in schizophrenia and bipolar disorder"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2815"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","The EMBO journal"],["dc.bibliographiccitation.lastpage","2828"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Pinheiro, Paulo S."],["dc.contributor.author","Rebola, Nelson"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Gertig, Michael"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Jatzko, Alexander"],["dc.contributor.author","Dettenhofer, Markus"],["dc.contributor.author","Zunszain, Patricia A"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Pape, Julius C"],["dc.contributor.author","Binder, Elisabeth B."],["dc.contributor.author","Mulle, Christophe"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2018-01-09T14:50:41Z"],["dc.date.available","2018-01-09T14:50:41Z"],["dc.date.issued","2017"],["dc.description.abstract","Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated memory decline that is further increased in the presence of additional risk factors and is mechanistically linked to a loss of transcriptional homeostasis. In conclusion, our data present a new approach to explore the connection between AD risk factors across life span and provide mechanistic insight to the processes by which neuropsychiatric diseases at a young age affect the risk for developing dementia."],["dc.identifier.doi","10.15252/embj.201796821"],["dc.identifier.pmid","28768717"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14923"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11608"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1460-2075"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","775"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The International Journal of Biochemistry & Cell Biology"],["dc.bibliographiccitation.lastpage","783"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Burkhardt, S."],["dc.contributor.author","Reiter, Russel J."],["dc.contributor.author","Tan, Dun-Xian"],["dc.contributor.author","Hardeland, Ruediger"],["dc.contributor.author","Cabrera, J. A."],["dc.contributor.author","Karbownik, M."],["dc.date.accessioned","2018-11-07T08:49:02Z"],["dc.date.available","2018-11-07T08:49:02Z"],["dc.date.issued","2001"],["dc.description.abstract","Chromium (Cr) compounds are widely used industrial chemicals and well known carcinogens. Cr(III) was earlier found to induce oxidative damage as documented by examining the levels of 8-hydroxydeoxyguanosine (8-OH-dG), an index for DNA damage, in isolated calf thymus DNA incubated with CrCl3 and H2O,. In the present in vitro study, we compared the ability of the free radical scavengers melatonin, N-1-acetyl-N-2-formyl-5-methoxykynuramine (AFMK), resveratrol and uric acid to reduce DNA damage induced by Cr(III). Each of these scavengers markedly reduced the DNA damage in a concentration-dependent manner. The concentrations that reduced 8-OH-dG formation by 50% (IC50) were 0.10 muM for both resveratrol and melatonin, and 0.27 muM for AFMK. However, the efficacy of the fourth endogenous antioxidant, i.e. uric acid, in terms of its inhibition of DNA damage in the same in vitro system was about 60-150 times less effective than the other scavengers; the IC50 for uric acid was 15.24 muM. These findings suggest that three of the four antioxidants tested in these studies may have utility in protecting against the environmental pollutant Cr and that the protective effects of these free radical scavengers against Cr(III)-induced carcinogenesis may relate to their direct hydroxyl radical scavenging ability. In the present study, the formation of 8-OH-dG was likely due to a Cr(III)-mediated Fenton-type reaction that generates hydroxyl radicals, which in turn damage DNA. Once formed, 8-OH-dG can mutate eventually leading to cancer; thus the implication is that these antioxidants may reduce the incidence of Cr-related cancers. (C) 2001 Published by Elsevier Science Ltd."],["dc.identifier.doi","10.1016/S1357-2725(01)00052-8"],["dc.identifier.isi","000170072700003"],["dc.identifier.pmid","11404181"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21358"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1357-2725"],["dc.title","DNA oxidatively damaged by chromium(III) and H2O2 is protected by the antioxidants melatonin, N-1-acetyl-N-2-formyl-5-methoxykynuramine, resveratrol and uric acid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5301"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Geochimica et Cosmochimica Acta"],["dc.bibliographiccitation.lastpage","5312"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Schulz, K. G."],["dc.contributor.author","Rost, Burkhard"],["dc.contributor.author","Burkhardt, S."],["dc.contributor.author","Riebesell, U."],["dc.contributor.author","Thoms, S."],["dc.contributor.author","Wolf-Gladrow, D. A."],["dc.date.accessioned","2018-11-07T10:53:23Z"],["dc.date.available","2018-11-07T10:53:23Z"],["dc.date.issued","2007"],["dc.description.abstract","Iron is limiting phytoplankton productivity in large parts of today's oceans, the so-called HNLC (high nutrient low chlorophyll) areas. It is a key component in photosynthesis during which inorganic carbon fixation in most phytoplankton species is sustained by so-called carbon concentrating mechanisms (CCMs). Here we investigate CCM regulation in the coccolithophore Emiliania huxleyi in response to varying degrees of iron limitation by means of membrane-inlet mass spectrometry. Compared to iron replete conditions rates of both active CO2 and HCO3- uptake were markedly reduced under iron limitation leading to significantly diminished growth rates. Moreover, there was a concomitant decrease in CCM efficiency, reflected in an increased CO2 loss from the cell in relation to carbon fixation. Under such conditions higher values for carbon isotope fractionation (epsilon(p)) would be expected. However, direct measurements of epsilon(p) showed that carbon isotope fractionation was insensitive to changes in growth rates and CCM activity. This can be explained by concomitant changes in internal DIC fluxes in and out of the chloroplast as demonstrated with a simple cell model comprising two compartments. Thus, carbon isotope fractionation reflects the ability of phytoplankton to actively control their inorganic carbon acquisition depending on environmental conditions. The insensitivity of carbon isotope fractionation to changes in the availability of iron could be of interest for paleoreconstructions in the HNLC areas of today's oceans. (c) 2007 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.gca.2007.09.012"],["dc.identifier.isi","000251052100002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49356"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0016-7037"],["dc.title","The effect of iron availability on the regulation of inorganic carbon acquisition in the coccolithophore Emiliania huxleyi and the significance of cellular compartmentation for stable carbon isotope fractionation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Schütz, Anna-Lena"],["dc.contributor.author","Irniger, Stefan"],["dc.contributor.author","Capece, Vincenzo"],["dc.date.accessioned","2018-04-11T16:20:54Z"],["dc.date.available","2018-04-11T16:20:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Although histone modifications and DNA methylation have been meticulously studied in the context of learning & memory formation, very few studies have demonstrated non-canonical histone variants as potential regulators of memory formation. Compared to canonical histones, these histone variants are expressed independently of DNA replication and are important for many physiological events as they confer altered chromatin structures, thereby regulating transcription. Recently, H2A.Z (variant of canonical histone, H2A) has been reported as a novel epigenetic regulator in memory formation (Zovkic et. al. 2014), which raised the question, whether differential binding of H2A.Z or its modification (e.g acetylation) across the whole genome could be a stable modulator for life-long memory acquisition and cognition. Here, we investigated genomic regions bound by H2A.Z and its acetylated variant (H2A.Zac) using chromatin immunoprecipitation followed by sequencing (ChIP-seq) in FACS-sorted neuronal and nonneuronal nuclei from hippocampal CA1 region. Initially, mRNA levels of H2afz (gene of H2A.Z) were assessed in CA1 region of aged (16 months old) and Alzheimer’s model mice (5XFAD) comparing them to young (3 months old) and wild type mice respectively. Furthermore, ChIP protocols for H2A.Z and H2A.Zac were optimized, as it has not been done before in this context. As a model of enhanced cognition, hippocampal CA1 regions from mice subjected to 4 months enriched environment (EE) were used for ChIP-seq against H2A.Z and H2A.Zac, comparing to home caged animals as controls. ChIP-seq analysis showed decreased binding of H2A.Z and its de-acetylation at specific promoter regions in CA1 neurons upon environmental enrichment. Promoters with decreased binding or decreased acetylation were found to be involved in genes functionally associated with neurogenesis, synaptic plasticity and several biosynthetic pathways. Further study is needed to prove their effect on transcription of those genes."],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13225"],["dc.language.iso","en"],["dc.notes.preprint","yes"],["dc.notes.status","final"],["dc.relation.eventend","4"],["dc.relation.eventlocation","Obergurgl, Austria"],["dc.relation.eventstart","28"],["dc.relation.iserratumof","yes"],["dc.title","Differential binding of non-canonical histone variant H2A.Z & its de-acetylation is evident in enhanced cognitive function"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3452"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","3464"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Kranz, Andrea"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Stewart, Adrian Francis"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:47:49Z"],["dc.date.available","2017-09-07T11:47:49Z"],["dc.date.issued","2013"],["dc.description.abstract","The consolidation of long-term memories requires differential gene expression. Recent research has suggested that dynamic changes in chromatin structure play a role in regulating the gene expression program linked to memory formation. The contribution of histone methylation, an important regulatory mechanism of chromatin plasticity that is mediated by the counteracting activity of histone-methyltransferases and histone-demethylases, is, however, not well understood. Here we show that mice lacking the histone-methyltransferase myeloid/lymphoid or mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult forebrain excitatory neurons display impaired hippocampus-dependent memory function. Consistent with the role of KMT2B in gene-activation DNA microarray analysis revealed that 152 genes were downregulated in the hippocampal dentate gyrus region of mice lacking kmt2b. Downregulated plasticity genes showed a specific deficit in histone 3 lysine 4 di-and trimethylation, while histone 3 lysine 4 monomethylation was not affected. Our data demonstrates that KMT2B mediates hippocampal histone 3 lysine 4 di-and trimethylation and is a critical player for memory formation."],["dc.identifier.doi","10.1523/JNEUROSCI.3356-12.2013"],["dc.identifier.gro","3142390"],["dc.identifier.isi","000315195700021"],["dc.identifier.pmid","23426673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7752"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Histone-Methyltransferase MLL2 (KMT2B) Is Required for Memory Formation in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","753"],["dc.bibliographiccitation.issue","5979"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","756"],["dc.bibliographiccitation.volume","328"],["dc.contributor.author","Peleg, Shahaf"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Zovoilis, Athanasios"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Cota, Perla"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Dettenhofer, Markus"],["dc.contributor.author","Kang, Hui"],["dc.contributor.author","Farinelli, Laurent"],["dc.contributor.author","Chen, Wei"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Doering, Aaron"],["dc.date.accessioned","2017-09-07T11:46:04Z"],["dc.date.available","2017-09-07T11:46:04Z"],["dc.date.issued","2010"],["dc.description.abstract","As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain."],["dc.identifier.doi","10.1126/science.1186088"],["dc.identifier.gro","3142928"],["dc.identifier.isi","000277357100040"],["dc.identifier.pmid","20448184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/386"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0036-8075"],["dc.title","Altered Histone Acetylation Is Associated with Age-Dependent Memory Impairment in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5062"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","5073"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Maddalena, Andrea"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Held, Torsten"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivanna"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2017-09-07T11:48:54Z"],["dc.date.available","2017-09-07T11:48:54Z"],["dc.date.issued","2012"],["dc.description.abstract","Histone acetylation has been implicated with the pathogenesis of neuropsychiatric disorders and targeting histone deacetylases (HDACs) using HDAC inhibitors was shown to be neuroprotective and to initiate neuroregenerative processes. However, little is known about the role of individual HDAC proteins during the pathogenesis of brain diseases. HDAC1 was found to be upregulated in patients suffering from neuropsychiatric diseases. Here, we show that virus-mediated overexpression of neuronal HDAC1 in the adult mouse hippocampus specifically affects the extinction of contextual fear memories, while other cognitive abilities were unaffected. In subsequent experiments we show that under physiological conditions, hippocampal HDAC1 is required for extinction learning via a mechanism that involves H3K9 deacetylation and subsequent trimethylation of target genes. In conclusion, our data show that hippocampal HDAC1 has a specific role in memory function."],["dc.identifier.doi","10.1523/JNEUROSCI.0079-12.2012"],["dc.identifier.gro","3142550"],["dc.identifier.isi","000302793500005"],["dc.identifier.pmid","22496552"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8913"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","HDAC1 Regulates Fear Extinction in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]