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000140291 0247_ $$2doi$$a10.1186/s40478-018-0611-4
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000140291 041__ $$aEnglish
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000140291 1001_ $$0P:(DE-HGF)0$$aMüller, Michaela Kerstin$$b0
000140291 245__ $$aNMDA receptors mediate synaptic depression, but not spine loss in the dentate gyrus of adult amyloid Beta (Aβ) overexpressing mice.
000140291 260__ $$aLondon$$bBiomed Central$$c2018
000140291 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2018-10-23
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000140291 520__ $$aAmyloid beta (Aβ)-mediated synapse dysfunction and spine loss are considered to be early events in Alzheimer's disease (AD) pathogenesis. N-methyl-D-aspartate receptors (NMDARs) have previously been suggested to play a role for Amyloid beta (Aβ) toxicity. Pharmacological block of NMDAR subunits in cultured neurons and mice suggested that NMDARs containing the GluN2B subunit are necessary for Aβ-mediated changes in synapse number and function in hippocampal neurons. Interestingly, NMDARs undergo a developmental switch from GluN2B- to GluN2A-containing receptors. This indicates different functional roles of NMDARs in young mice compared to older animals. In addition, the lack of pharmacological tools to efficiently dissect the role of NMDARs containing the different subunits complicates the interpretation of their specific role. In order to address this problem and to investigate the specific role for Aβ toxicity of the distinct NMDAR subunits in dentate gyrus granule cells of adult mice, we used conditional knockout mouse lines for the subunits GluN1, GluN2A and GluN2B. Aβ-mediated changes in synaptic function and neuronal anatomy were investigated in several-months old mice with virus-mediated overproduction of Aβ and in 1-year old 5xFAD mice. We found that all three NMDAR subunits contribute to the Aβ-mediated decrease in the number of functional synapses. However, NMDARs are not required for the spine number reduction in dentate gyrus granule cells after chronic Aβ-overproduction in 5xFAD mice. Furthermore, the amplitude of synaptic and extrasynaptic NMDAR-mediated currents was reduced in dentate gyrus granule of 5xFAD mice without changes in current kinetics, suggesting that a redistribution or change in subunit composition of NMDARs does not play a role in mediating Amyloid beta (Aβ) toxicity. Our study indicates that NMDARs are involved in AD pathogenesis by compromising synapse function but not by affecting neuron morphology.
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000140291 542__ $$2Crossref$$i2018-10-23$$uhttp://creativecommons.org/licenses/by/4.0/
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000140291 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000140291 650_7 $$2NLM Chemicals$$aAmyloid beta-Protein Precursor
000140291 650_7 $$2NLM Chemicals$$aExcitatory Amino Acid Agents
000140291 650_7 $$2NLM Chemicals$$aPSEN1 protein, human
000140291 650_7 $$2NLM Chemicals$$aPresenilin-1
000140291 650_7 $$2NLM Chemicals$$aReceptors, N-Methyl-D-Aspartate
000140291 650_7 $$0EC 2.7.11.17$$2NLM Chemicals$$aCalcium-Calmodulin-Dependent Protein Kinase Type 2
000140291 650_2 $$2MeSH$$aAction Potentials: drug effects
000140291 650_2 $$2MeSH$$aAction Potentials: genetics
000140291 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000140291 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000140291 650_2 $$2MeSH$$aAmyloid beta-Peptides: chemistry
000140291 650_2 $$2MeSH$$aAmyloid beta-Peptides: genetics
000140291 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000140291 650_2 $$2MeSH$$aAmyloid beta-Peptides: pharmacology
000140291 650_2 $$2MeSH$$aAmyloid beta-Protein Precursor: genetics
000140291 650_2 $$2MeSH$$aAnimals
000140291 650_2 $$2MeSH$$aCalcium-Calmodulin-Dependent Protein Kinase Type 2: genetics
000140291 650_2 $$2MeSH$$aCalcium-Calmodulin-Dependent Protein Kinase Type 2: metabolism
000140291 650_2 $$2MeSH$$aDendritic Spines: pathology
000140291 650_2 $$2MeSH$$aDentate Gyrus: cytology
000140291 650_2 $$2MeSH$$aDisease Models, Animal
000140291 650_2 $$2MeSH$$aExcitatory Amino Acid Agents: pharmacology
000140291 650_2 $$2MeSH$$aExcitatory Postsynaptic Potentials: drug effects
000140291 650_2 $$2MeSH$$aExcitatory Postsynaptic Potentials: genetics
000140291 650_2 $$2MeSH$$aFemale
000140291 650_2 $$2MeSH$$aGene Expression Regulation: drug effects
000140291 650_2 $$2MeSH$$aGene Expression Regulation: genetics
000140291 650_2 $$2MeSH$$aHEK293 Cells
000140291 650_2 $$2MeSH$$aHumans
000140291 650_2 $$2MeSH$$aMale
000140291 650_2 $$2MeSH$$aMice
000140291 650_2 $$2MeSH$$aMice, Inbred C57BL
000140291 650_2 $$2MeSH$$aMice, Transgenic
000140291 650_2 $$2MeSH$$aMutation: genetics
000140291 650_2 $$2MeSH$$aNeurons: drug effects
000140291 650_2 $$2MeSH$$aNeurons: physiology
000140291 650_2 $$2MeSH$$aNeurons: ultrastructure
000140291 650_2 $$2MeSH$$aPresenilin-1: genetics
000140291 650_2 $$2MeSH$$aReceptors, N-Methyl-D-Aspartate: genetics
000140291 650_2 $$2MeSH$$aReceptors, N-Methyl-D-Aspartate: metabolism
000140291 650_2 $$2MeSH$$aSynapses: drug effects
000140291 650_2 $$2MeSH$$aSynapses: physiology
000140291 7001_ $$0P:(DE-HGF)0$$aJacobi, Eric$$b1
000140291 7001_ $$0P:(DE-HGF)0$$aSakimura, Kenji$$b2
000140291 7001_ $$0P:(DE-HGF)0$$aMalinow, Roberto$$b3
000140291 7001_ $$0P:(DE-2719)2810460$$aEngelhardt, Jakob$$b4$$eLast author$$udzne
000140291 77318 $$2Crossref$$3journal-article$$a10.1186/s40478-018-0611-4$$b : Springer Science and Business Media LLC, 2018-10-23$$n1$$p110$$tActa Neuropathologica Communications$$v6$$x2051-5960$$y2018
000140291 773__ $$0PERI:(DE-600)2715589-4$$a10.1186/s40478-018-0611-4$$gVol. 6, no. 1, p. 110$$n1$$p110$$q6:1<110$$tActa Neuropathologica Communications$$v6$$x2051-5960$$y2018
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000140291 999C5 $$2Crossref$$9-- missing cx lookup --$$a10.1016/j.neuron.2011.09.023$$o10.1016/j.neuron.2011.09.023
000140291 999C5 $$2Crossref$$9-- missing cx lookup --$$a10.1006/exnr.1999.7085$$o10.1006/exnr.1999.7085
000140291 999C5 $$2Crossref$$9-- missing cx lookup --$$a10.1097/00001756-199212000-00027$$o10.1097/00001756-199212000-00027
000140291 999C5 $$2Crossref$$9-- missing cx lookup --$$a10.1038/nn.2476$$o10.1038/nn.2476
000140291 999C5 $$2Crossref$$9-- missing cx lookup --$$a10.1002/(SICI)1099-1166(199902)14:2<135::AID-GPS906>3.0.CO;2-0$$o10.1002/(SICI)1099-1166(199902)14:2<135::AID-GPS906>3.0.CO;2-0
000140291 999C5 $$2Crossref$$9-- missing cx lookup --$$a10.1038/cddis.2013.82$$o10.1038/cddis.2013.82