Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/80487
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dc.contributorDepartment of Rehabilitation Sciences-
dc.creatorYau, SYen_US
dc.creatorBettio, Len_US
dc.creatorChiu, Jen_US
dc.creatorChiu, Cen_US
dc.creatorChristie, BRen_US
dc.date.accessioned2019-03-26T09:17:29Z-
dc.date.available2019-03-26T09:17:29Z-
dc.identifier.urihttp://hdl.handle.net/10397/80487-
dc.language.isoenen_US
dc.publisherFrontiers Media SAen_US
dc.rightsCopyright © 2019 Yau, Bettio, Chiu, Chiu and Christie. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) (https://creativecommons.org/licenses/by/4.0/). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en_US
dc.rightsThe following publication Yau, S. Y., Bettio, L., Chiu, J., Chiu, C., & Christie, B. R. (2019). Fragile-X syndrome is associated with NMDA receptor hypofunction and reduced dendritic complexity in mature dentate granule cells. Frontiers in Molecular Neuroscience, 11, 495, 1-10 is available at https://dx.doi.org/10.3389/fnmol.2018.00495en_US
dc.subjectFragile X syndrome (FXS)en_US
dc.subjectNMDA (N-methy-D-aspartate receptor)en_US
dc.subjectDendrite complexityen_US
dc.subjectNeurogenesisen_US
dc.subjectDentate gyrusen_US
dc.subjectAMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)en_US
dc.titleFragile-X syndrome is associated with NMDA receptor hypofunction and reduced dendritic complexity in mature dentate granule cellsen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1en_US
dc.identifier.epage10en_US
dc.identifier.volume11en_US
dc.identifier.doi10.3389/fnmol.2018.00495en_US
dcterms.abstractFragile X syndrome (FXS) is the most common form of inherited intellectual disability. It is caused by the overexpansion of cytosine-guanine-guanine (CGG) trinucleotide in Fmr1 gene, resulting in complete loss of the fragile X mental retardation protein (FMRP). Previous studies using Fmr1 knockout (Fmr1 KO) mice have suggested that a N-methyl-D-aspartate receptors (NMDAR) hypofunction in the hippocampal dentate gyrus may partly contribute to cognitive impairments in FXS. Since activation of NMDAR plays an important role in dendritic arborization during neuronal development, we examined whether deficits in NMDAR function are associated with alterations in dendritic complexity in the hippocampal dentate region. The dentate granule cell layer (GCL) presents active postnatal neurogenesis, and consists of a heterogenous neuronal population with gradient ages from the superficial to its deep layer. Here, we show that neurons with multiple primary dendrites that reside in the outer GCL of Fmr1 KO mice display significantly smaller NMDAR excitatory post-synaptic currents (EPSCs) and a higher alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) to NMDA ratio in comparison to their wild-type counterparts. These deficits were associated with a significant decrease in dendritic complexity, with both dendritic length and number of intersections being significantly reduced. In contrast, although neurons with a single primary dendrite resided in the inner GCL of Fmr1 KO mice had a trend toward a reduction in NMDAR EPSCs and a higher AMPA/NMDA ratio, no alterations were found in dendritic complexity at this developmental stage. Our data indicate that the loss of FMRP causes NMDAR deficits and reduced dendritic complexity in granule neurons with multiple primary dendrites which are thought to be more mature in the GCL.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationFrontiers in molecular neuroscience, 17 Jan. 2019, v. 11, 495, p. 1-10en_US
dcterms.isPartOfFrontiers in molecular neuroscienceen_US
dcterms.issued2019-01-17-
dc.identifier.isiWOS:000456000600001-
dc.identifier.eissn1662-5099en_US
dc.identifier.artn495en_US
dc.description.validate201903 bcrc-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumbera0763-n15en_US
dc.identifier.SubFormID1508en_US
dc.description.fundingSourceSelf-fundeden_US
dc.description.pubStatusPublisheden_US
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