Dean, Camin

[["dc.bibliographiccitation.firstpage","106"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Hippocampus"],["dc.bibliographiccitation.lastpage","118"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Zafar, Noman"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-11-07T10:04:08Z"],["dc.date.available","2018-11-07T10:04:08Z"],["dc.date.issued","2015"],["dc.description.abstract","Ethanol inhibits memory encoding and the induction of long-term potentiation (LTP) in CA1 neurons of the hippocampus. Hippocampal LTP at Schaffer collateral synapses onto CA1 pyramidal neurons has been widely studied as a cellular model of learning and memory, but there is striking heterogeneity in the underlying molecular mechanisms in distinct regions and in response to distinct stimuli. Basal and apical dendrites differ in terms of innervation, input specificity, and molecular mechanisms of LTP induction and maintenance, and different stimuli determine distinct molecular pathways of potentiation. However, lamina or stimulus-dependent effects of ethanol on LTP have not been investigated. Here, we tested the effect of acute application of 60 mM ethanol on LTP induction in distinct dendritic compartments (apical versus basal) of CA1 neurons, and in response to distinct stimulation paradigms (single versus repeated, spaced high frequency stimulation). We found that ethanol completely blocks LTP in apical dendrites, whereas it reduces the magnitude of LTP in basal dendrites. Acute ethanol treatment for just 15 min altered pre- and post-synaptic protein expression. Interestingly, ethanol increases the neurosteroid allopregnanolone, which causes ethanol-dependent inhibition of LTP, more prominently in apical dendrites, where ethanol has greater effects on LTP. This suggests that ethanol has general effects on fundamental properties of synaptic plasticity, but the magnitude of its effect on LTP differs depending on hippocampal sub-region and stimulus strength. (c) 2014 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/hipo.22356"],["dc.identifier.isi","000346255600010"],["dc.identifier.pmid","25155179"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38630"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1063"],["dc.relation.issn","1050-9631"],["dc.title","Ethanol Inhibits Long-Term Potentiation in Hippocampal CA1 Neurons, Irrespective of Lamina and Stimulus Strength, Through Neurosteroidogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","eaav1483"],["dc.bibliographiccitation.issue","6422"],["dc.bibliographiccitation.journal","Science (New York, N.Y.)"],["dc.bibliographiccitation.volume","363"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Shinoda, Yo"],["dc.contributor.author","Nitzan, Noam"],["dc.contributor.author","Heukamp, Alina"],["dc.contributor.author","Rannio, Sabine"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Wang, Yu Tian"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-31T13:02:46Z"],["dc.date.available","2019-07-31T13:02:46Z"],["dc.date.issued","2019"],["dc.description.abstract","Forgetting is important. Without it, the relative importance of acquired memories in a changing environment is lost. We discovered that synaptotagmin-3 (Syt3) localizes to postsynaptic endocytic zones and removes AMPA receptors from synaptic plasma membranes in response to stimulation. AMPA receptor internalization, long-term depression (LTD), and decay of long-term potentiation (LTP) of synaptic strength required calcium-sensing by Syt3 and were abolished through Syt3 knockout. In spatial memory tasks, mice in which Syt3 was knocked out learned normally but exhibited a lack of forgetting. Disrupting Syt3:GluA2 binding in a wild-type background mimicked the lack of LTP decay and lack of forgetting, and these effects were occluded in the Syt3 knockout background. Our findings provide evidence for a molecular mechanism in which Syt3 internalizes AMPA receptors to depress synaptic strength and promote forgetting."],["dc.identifier.doi","10.1126/science.aav1483"],["dc.identifier.pmid","30545844"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62245"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.issn","1095-9203"],["dc.title","Synaptotagmin-3 drives AMPA receptor endocytosis, depression of synapse strength, and forgetting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3572"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","3584"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Haider, Rashi"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Navarro-Sala, Magdalena"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Schuetz, Anna-Lena"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Luehrmann, Reinhard"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:43:34Z"],["dc.date.available","2017-09-07T11:43:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Aging and increased amyloid burden are major risk factors for cognitive diseases such as Alzheimer's disease (AD). Effective therapies for these diseases are lacking. Here, we evaluated mouse models of age-associated memory impairment and amyloid deposition to study transcriptome and cell type-specific epigenome plasticity in the brain and peripheral organs. We determined that aging and amyloid pathology are associated with inflammation and impaired synaptic function in the hippocampal CA1 region as the result of epigenetic-dependent alterations in gene expression. In both amyloid and aging models, inflammation was associated with increased gene expression linked to a subset of transcription factors, while plasticity gene deregulation was differentially mediated. Amyloid pathology impaired histone acetylation and decreased expression of plasticity genes, while aging altered H4K12 acetylation-linked differential splicing at the intron-exon junction in neurons, but not nonneuronal cells. Furthermore, oral administration of the clinically approved histone deacetylase inhibitor vorinostat not only restored spatial memory, but also exerted antiinflammatory action and reinstated epigenetic balance and transcriptional homeostasis at the level of gene expression and exon usage. This study provides a systems-level investigation of transcriptome plasticity in the hippocampal CA1 region in aging and AD models and suggests that histone deacetylase inhibitors should be further explored as a cost-effective therapeutic strategy against age-associated cognitive decline."],["dc.identifier.doi","10.1172/JCI79942"],["dc.identifier.gro","3141833"],["dc.identifier.isi","000362303600031"],["dc.identifier.pmid","26280576"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1579"],["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","1558-8238"],["dc.relation.issn","0021-9738"],["dc.title","HDAC inhibitor-dependent transcriptome and memory reinstatement in cognitive decline models"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","546"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","554"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Pena-Centeno, Tonatiuh"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Zhou, Qihui"],["dc.contributor.author","Edbauer, Dieter"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2020-12-10T14:23:00Z"],["dc.date.available","2020-12-10T14:23:00Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.celrep.2018.03.059"],["dc.identifier.issn","2211-1247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71800"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","RNA-Dependent Intergenerational Inheritance of Enhanced Synaptic Plasticity after Environmental Enrichment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5842"],["dc.bibliographiccitation.issue","30"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","5860"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Markworth, Ronja"],["dc.contributor.author","Adolfs, Youri"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Steinbeck, Lars M."],["dc.contributor.author","Lizé, Muriel"],["dc.contributor.author","Pasterkamp, R. Jeroen"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Burk, Katja"],["dc.date.accessioned","2020-12-10T18:42:33Z"],["dc.date.available","2020-12-10T18:42:33Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1523/JNEUROSCI.0027-19.2019"],["dc.identifier.eissn","1529-2401"],["dc.identifier.issn","0270-6474"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78005"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Sensory Axon Growth Requires Spatiotemporal Integration of CaSR and TrkB Signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","521"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","533"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Körber, Christoph"],["dc.contributor.author","Horstmann, Heinz"],["dc.contributor.author","Venkataramani, Varun"],["dc.contributor.author","Herrmannsdörfer, Frank"],["dc.contributor.author","Kremer, Thomas"],["dc.contributor.author","Kaiser, Michaela"],["dc.contributor.author","Schwenger, Darius B."],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Dresbach, Thomas"],["dc.contributor.author","Kuner, Thomas"],["dc.date.accessioned","2018-09-28T09:27:35Z"],["dc.date.available","2018-09-28T09:27:35Z"],["dc.date.issued","2015"],["dc.description.abstract","Mover, a member of the exquisitely small group of vertebrate-specific presynaptic proteins, has been discovered as an interaction partner of the scaffolding protein Bassoon, yet its function has not been elucidated. We used adeno-associated virus (AAV)-mediated shRNA expression to knock down Mover in the calyx of Held in vivo. Although spontaneous synaptic transmission remained unaffected, we found a strong increase of the evoked EPSC amplitude. The size of the readily releasable pool was unaltered, but short-term depression was accelerated and enhanced, consistent with an increase in release probability after Mover knockdown. This increase in release probability was not caused by alterations in Ca(2+) influx but rather by a higher Ca(2+) sensitivity of the release machinery, as demonstrated by presynaptic Ca(2+) uncaging. We therefore conclude that Mover expression in certain subsets of synapses negatively regulates synaptic release probability, constituting a novel mechanism to tune synaptic transmission."],["dc.identifier.doi","10.1016/j.neuron.2015.07.001"],["dc.identifier.pmid","26212709"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15842"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.eissn","1097-4199"],["dc.title","Modulation of Presynaptic Release Probability by the Vertebrate-Specific Protein Mover"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1087"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cerebral Cortex"],["dc.bibliographiccitation.lastpage","1104"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Hurtado-Zavala, Joaquin I"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Faram, Ruth"],["dc.contributor.author","Ahmad, Hamid"],["dc.contributor.author","Swaminathan, Aarti"],["dc.contributor.author","McIlhinney, Jeffrey"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Perestenko, Pavel"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-01-09T14:34:30Z"],["dc.date.available","2018-01-09T14:34:30Z"],["dc.date.issued","2017"],["dc.description.abstract","Dendritic spines compartmentalize information in the brain, and their morphological characteristics are thought to underly synaptic plasticity. Here we identify copine-6 as a novel modulator of dendritic spine morphology. We found that brain-derived neurotrophic factor (BDNF) - a molecule essential for long-term potentiation of synaptic strength - upregulated and recruited copine-6 to dendritic spines in hippocampal neurons. Overexpression of copine-6 increased mushroom spine number and decreased filopodia number, while copine-6 knockdown had the opposite effect and dramatically increased the number of filopodia, which lacked PSD95. Functionally, manipulation of post-synaptic copine-6 levels affected miniature excitatory post-synaptic current (mEPSC) kinetics and evoked synaptic vesicle recycling in contacting boutons, and post-synaptic knockdown of copine-6 reduced hippocampal LTP and increased LTD. Mechanistically, copine-6 promotes BDNF-TrkB signaling and recycling of activated TrkB receptors back to the plasma membrane surface, and is necessary for BDNF-induced increases in mushroom spines in hippocampal neurons. Thus copine-6 regulates BDNF-dependent changes in dendritic spine morphology to promote synaptic plasticity."],["dc.identifier.doi","10.1093/cercor/bhx009"],["dc.identifier.pmid","28158493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11602"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1460-2199"],["dc.title","Regulation of Dendritic Spine Morphology in Hippocampal Neurons by Copine-6"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]