Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/66464
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dc.contributorDepartment of Rehabilitation Sciencesen_US
dc.creatorYau, SYen_US
dc.creatorBostrom, CAen_US
dc.creatorChiu, Jen_US
dc.creatorFontaine, CJen_US
dc.creatorSawchuk, Sen_US
dc.creatorMeconi, Aen_US
dc.creatorWortman, RCen_US
dc.creatorTruesdell, Een_US
dc.creatorTruesdell, Aen_US
dc.creatorChiu, Cen_US
dc.creatorHryciw, BNen_US
dc.creatorEadie, BDen_US
dc.creatorGhilan, Men_US
dc.creatorChristie, BRen_US
dc.date.accessioned2017-05-22T02:26:11Z-
dc.date.available2017-05-22T02:26:11Z-
dc.identifier.issn0969-9961en_US
dc.identifier.urihttp://hdl.handle.net/10397/66464-
dc.language.isoenen_US
dc.publisherAcademic Pressen_US
dc.rights© 2016 Elsevier Inc. All rights reserved.en_US
dc.rights© 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.rightsThe following publication Yau, S. Y., Bostrom, C. A., Chiu, J., Fontaine, C. J., Sawchuk, S., Meconi, A., ... & Christie, B. R. (2016). Impaired bidirectional NMDA receptor dependent synaptic plasticity in the dentate gyrus of adult female Fmr1 heterozygous knockout mice. Neurobiology of disease, 96, 261-270 is available at https://doi.org/10.1016/j.nbd.2016.09.012.en_US
dc.subjectFragile X syndromeen_US
dc.subjectFemalesen_US
dc.subjectHippocampusen_US
dc.subjectLearning and memoryen_US
dc.subjectSynaptic plasticityen_US
dc.titleImpaired bidirectional NMDA receptor dependent synaptic plasticity in the dentate gyrus of adult female Fmrl heterozygous knockout miceen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage261en_US
dc.identifier.epage270en_US
dc.identifier.volume96en_US
dc.identifier.doi10.1016/j.nbd.2016.09.012en_US
dcterms.abstractFragile-X syndrome (FXS) is caused by the transcriptional repression of the Fmrl gene resulting in loss of the Fragile-X mental retardation protein (FMRP). This leads to cognitive impairment in both male and female patients, however few studies have focused on the impact of FXS in females. Significant cognitive impairment has been reported in approximately 35% of women who exhibit a heterozygous Fmrl gene mutation, however to date there is a paucity of information regarding the mechanistic underpinnings of these deficits. We, and others, have recently reported that there is significant impairment in N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) and long-term depression (LTD) in the hippocampal dentate gyrus (DG) of male Fmrl knock out mice. Here we examined if female mice displaying a heterozygous loss of the Fmrl gene (Fmr1(+/-)) would exhibit similar impairments in DG-dependent spatial memory processing and NMDAR hypofunction. We found that Female Fmr1(+/-) mice did not show impaired metabotropic glutamate receptor (mGluR)-LTD in the CA1 region, and could perform well on a temporal ordering task that is thought to involve this brain region. In contrast, female Fmr1+/- mice showed impairments in a pattern separation task thought to involve the DG, and also displayed a significant impairment in both NMDAR-dependent LTD and LTP in this region. The LTP impairment could be rescued by administering the NMDAR co-agonist, glycine. Our data suggests that NMDAR hypofunction in the DG may partly contribute to learning and memory impairment in female Fmr1(+/-) mice. Targeting NMDAR-dependent mechanisms may offer hope as a new therapeutic approach for treating female FXS patients with learning and memory impairments.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationNeurobiology of disease, Dec. 2016, v. 96, p. 261-270en_US
dcterms.isPartOfNeurobiology of diseaseen_US
dcterms.issued2016-12-
dc.identifier.isiWOS:000388058900024-
dc.identifier.pmid27659109-
dc.identifier.ros2016003438-
dc.identifier.eissn1095-953Xen_US
dc.identifier.rosgroupid2016003369-
dc.description.ros2016-2017 > Academic research: refereed > Publication in refereed journalen_US
dc.description.validate201804_a bcmaen_US
dc.description.oaAccepted Manuscripten_US
dc.identifier.FolderNumberRS-0418, a0763-n24-
dc.identifier.SubFormID1520-
dc.description.fundingSourceOthersen_US
dc.description.fundingTextCanadian Institutes for Health Research; postdoctoral fellowship awarded to SY Yau by the CIHR in partnership of Fragile X Research Foundation of Canadaen_US
dc.description.pubStatusPublisheden_US
dc.identifier.OPUS6680765-
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