Favaro, Plinio D.

[["dc.bibliographiccitation.firstpage","15504"],["dc.bibliographiccitation.issue","39"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","15517"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Krueger, Juliane M."],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Liu, Mingna"],["dc.contributor.author","Kitlinska, Agata"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Raabe, Monika"],["dc.contributor.author","Akad, Derya S."],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Xu, Weifeng"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:19:47Z"],["dc.date.available","2018-11-07T09:19:47Z"],["dc.date.issued","2013"],["dc.description.abstract","In the postsynaptic density of glutamatergic synapses, the discs large (DLG)-membrane-associated guanylate kinase (MAGUK) family of scaffolding proteins coordinates a multiplicity of signaling pathways to maintain and regulate synaptic transmission. Postsynaptic density-93 (PSD-93) is the most variable paralog in this family; it exists in six different N-terminal isoforms. Probably because of the structural and functional variability of these isoforms, the synaptic role of PSD-93 remains controversial. To accurately characterize the synaptic role of PSD-93, we quantified the expression of all six isoforms in the mouse hippocampus and examined them individually in hippocampal synapses. Using molecular manipulations, including overexpression, gene knockdown, PSD-93 knock-out mice combined with biochemical assays, and slice electrophysiology both in rat and mice, we demonstrate that PSD-93 is required at different developmental synaptic states to maintain the strength of excitatory synaptic transmission. This strength is differentially regulated by the six isoforms of PSD-93, including regulations of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-active and inactive synapses, and activity-dependent modulations. Collectively, these results demonstrate that alternative combinations of N-terminal PSD-93 isoforms and DLG-MAGUK paralogs can fine-tune signaling scaffolds to adjust synaptic needs to regulate synaptic transmission."],["dc.identifier.doi","10.1523/JNEUROSCI.0019-12.2013"],["dc.identifier.isi","000324912500021"],["dc.identifier.pmid","24068818"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28724"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Differential Roles of Postsynaptic Density-93 Isoforms in Regulating Synaptic Transmission"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","95"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of High Energy Physics"],["dc.bibliographiccitation.volume","2022"],["dc.contributor.author","Patra, S."],["dc.contributor.author","Bhardwaj, V."],["dc.contributor.author","Trabelsi, K."],["dc.contributor.author","Adachi, I."],["dc.contributor.author","Aihara, H."],["dc.contributor.author","Al Said, S."],["dc.contributor.author","Asner, D. M."],["dc.contributor.author","Atmacan, H."],["dc.contributor.author","Aushev, T."],["dc.contributor.author","Ayad, R."],["dc.contributor.author","Das, S."],["dc.contributor.author","Frey, A."],["dc.contributor.author","Hernandez, M."],["dc.contributor.author","Jin, Y."],["dc.contributor.author","Li, J."],["dc.contributor.author","Li, Y."],["dc.contributor.author","Paul, S."],["dc.contributor.authorgroup","The BELLE collaboration"],["dc.date.accessioned","2022-06-01T09:39:15Z"],["dc.date.accessioned","2022-08-16T12:38:16Z"],["dc.date.available","2022-06-01T09:39:15Z"],["dc.date.available","2022-08-16T12:38:16Z"],["dc.date.issued","2022-05-16"],["dc.date.updated","2022-07-29T11:35:17Z"],["dc.description.abstract","Abstract\r\n \r\n We present a search for the charged lepton-flavor-violating decays ϒ(1S) → ℓ±ℓ′∓ and radiative charged lepton-flavour-violating decays ϒ(1S) → γℓ±ℓ′∓ [ℓ,ℓ′ = e, μ, τ] using the 158 million ϒ(2S) sample collected by the Belle detector at the KEKB collider. This search uses ϒ(1S) mesons produced in ϒ(2S) → π+π− ϒ(1S) transitions. We do not find any significant signal, so we provide upper limits on the branching fractions at the 90% confidence level."],["dc.identifier.citation","Journal of High Energy Physics. 2022 May 16;2022(5):95"],["dc.identifier.doi","10.1007/JHEP05(2022)095"],["dc.identifier.pii","18383"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108422"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112737"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1029-8479"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","e\r\n +-e\r\n − Experiments"],["dc.title","Search for charged lepton flavor violating decays of ϒ (1S)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2006838"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLOS Biology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Stodieck, Sophia"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Liu, Yu-Zhang"],["dc.contributor.author","Engelhardt, Karl-Alexander"],["dc.contributor.author","Schmitz, Frank"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Schlüter, Oliver M."],["dc.date.accessioned","2019-07-09T11:49:59Z"],["dc.date.available","2019-07-09T11:49:59Z"],["dc.date.issued","2018"],["dc.description.abstract","The disc-large (DLG)-membrane-associated guanylate kinase (MAGUK) family of proteins forms a central signaling hub of the glutamate receptor complex. Among this family, some proteins regulate developmental maturation of glutamatergic synapses, a process vulnerable to aberrations, which may lead to neurodevelopmental disorders. As is typical for paralogs, the DLG-MAGUK proteins postsynaptic density (PSD)-95 and PSD-93 share similar functional domains and were previously thought to regulate glutamatergic synapses similarly. Here, we show that they play opposing roles in glutamatergic synapse maturation. Specifically, PSD-95 promoted, whereas PSD-93 inhibited maturation of immature α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-type glutamate receptor (AMPAR)-silent synapses in mouse cortex during development. Furthermore, through experience-dependent regulation of its protein levels, PSD-93 directly inhibited PSD-95's promoting effect on silent synapse maturation in the visual cortex. The concerted function of these two paralogs governed the critical period of juvenile ocular dominance plasticity (jODP), and fine-tuned visual perception during development. In contrast to the silent synapse-based mechanism of adjusting visual perception, visual acuity improved by different mechanisms. Thus, by controlling the pace of silent synapse maturation, the opposing but properly balanced actions of PSD-93 and PSD-95 are essential for fine-tuning cortical networks for receptive field integration during developmental critical periods, and imply aberrations in either direction of this process as potential causes for neurodevelopmental disorders."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.1371/journal.pbio.2006838"],["dc.identifier.pmid","30586380"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15797"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59674"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.ddc","612"],["dc.title","An opposing function of paralogs in balancing developmental synapse maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1150"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","1155"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Greifzu, Franziska"],["dc.contributor.author","Pielecka-Fortuna, Justyna"],["dc.contributor.author","Kalogeraki, Evgenia"],["dc.contributor.author","Krempler, Katja"],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Schlueter, Oliver M."],["dc.contributor.author","Loewel, Siegrid"],["dc.date.accessioned","2018-11-07T09:45:04Z"],["dc.date.available","2018-11-07T09:45:04Z"],["dc.date.issued","2014"],["dc.description.abstract","Ocular dominance (OD) plasticity in mouse primary visual cortex (V1) declines during postnatal development and is absent beyond postnatal day 110 if mice are raised in standard cages (SCs). An enriched environment (EE) promotes OD plasticity in adult rats. Here, we explored cellular mechanisms of EE in mouse V1 and the therapeutic potential of EE to prevent impairments of plasticity after a cortical stroke. Using in vivo optical imaging, we observed that monocular deprivation in adult EE mice (i) caused a very strong OD plasticity previously only observed in 4-wk-old animals, (ii) restored already lost OD plasticity in adult SC-raised mice, and (iii) preserved OD plasticity after a stroke in the primary somatosensory cortex. Using patch-clamp electrophysiology in vitro, we also show that (iv) local inhibition was significantly reduced in V1 slices of adult EE mice and (v) the GABA/AMPA ratio was like that in 4-wk-old SC-raised animals. These observations were corroborated by in vivo analyses showing that diazepam treatment significantly reduced the OD shift of EE mice after monocular deprivation. Taken together, EE extended the sensitive phase for OD plasticity into late adulthood, rejuvenated V1 after 4 mo of SC-rearing, and protected adult mice from stroke-induced impairments of cortical plasticity. The EE effect was mediated most likely by preserving low juvenile levels of inhibition into adulthood, which potentially promoted adaptive changes in cortical circuits."],["dc.identifier.doi","10.1073/pnas.1313385111"],["dc.identifier.isi","000329928400065"],["dc.identifier.pmid","24395770"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34536"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]