PSD95 suppresses dendritic arbor development in mature hippocampal neurons by occluding the clustering of NR2B-NMDA receptors

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dc.contributor.authorBustos, Fernando J.
dc.contributor.authorVarela-Nallar, Lorena
dc.contributor.authorCampos, Matias
dc.contributor.authorHenriquez, Berta
dc.contributor.authorPhillips, Marnie
dc.contributor.authorOpazo, Carlos
dc.contributor.authorAguayo, Luis G.
dc.contributor.authorMontecino, Martin
dc.contributor.authorConstantine-Paton, Martha
dc.contributor.authorInestrosa, Nibaldo C.
dc.contributor.authorVan Zundert, Brigitte
dc.date.accessioned2023-06-13T17:59:34Z
dc.date.available2023-06-13T17:59:34Z
dc.date.issued2014-04
dc.descriptionIndexación Scopus.es
dc.description.abstractConsiderable evidence indicates that the NMDA receptor (NMDAR) subunits NR2A and NR2B are critical mediators of synaptic plasticity and dendritogenesis; however, how they differentially regulate these processes is unclear. Here we investigate the roles of the NR2A and NR2B subunits, and of their scaffolding proteins PSD-95 and SAP102, in remodeling the dendritic architecture of developing hippocampal neurons (2–25 DIV). Analysis of the dendritic architecture and the temporal and spatial expression patterns of the NMDARs and anchoring proteins in immature cultures revealed a strong positive correlation between synaptic expression of the NR2B subunit and dendritogenesis. With maturation, the pruning of dendritic branches was paralleled by a strong reduction in overall and synaptic expression of NR2B, and a significant elevation in synaptic expression of NR2A and PSD95. Using constructs that alter the synaptic composition, we found that either over-expression of NR2B or knock-down of PSD95 by shRNA-PSD95 augmented dendritogenesis in immature neurons. Reactivation of dendritogenesis could also be achieved in mature cultured neurons, but required both manipulations simultaneously, and was accompanied by increased dendritic clustering of NR2B. Our results indicate that the developmental increase in synaptic expression of PSD95 obstructs the synaptic clustering of NR2B-NMDARs, and thereby restricts reactivation of dendritic branching. Experiments with shRNA-PSD95 and chimeric NR2A/NR2B constructs further revealed that C-terminus of the NR2B subunit (tail) was sufficient to induce robust dendritic branching in mature hippocampal neurons, and suggest that the NR2B tail is important in recruiting calcium-dependent signaling proteins and scaffolding proteins necessary for dendritogenesis.es
dc.description.urihttps://journals.plos.org/plosone/article/authors?id=10.1371/journal.pone.0094037
dc.identifier.citationPLoS ONE. Volume 9, Issue 4. 4 April 2014. Article number e94037es
dc.identifier.doiDOI: 10.1371/journal.pone.0094037
dc.identifier.issn1932-6203
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/50635
dc.language.isoenes
dc.publisherPublic Library of Sciencees
dc.rights.licenseAtribution 4.0 International (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subjectNeuronal Dendriteses
dc.subjectHippocampuses
dc.subjectNeuronses
dc.subjectTransfectiones
dc.subjectDevelopmental Neurosciencees
dc.subjectSpinal Cordes
dc.subjectDendritic Structurees
dc.subjectSynapseses
dc.titlePSD95 suppresses dendritic arbor development in mature hippocampal neurons by occluding the clustering of NR2B-NMDA receptorses
dc.typeArtículoes
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