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dc.contributor.authorLi, Qin
dc.contributor.authorNavakkode, Sheeja
dc.contributor.authorRothkegel, Martin
dc.contributor.authorSoong, Tuck Wah
dc.contributor.authorSajikumar, Sreedharan
dc.contributor.authorKorte, Martin
dc.date.accessioned2017-12-08T15:17:03Z
dc.date.available2017-12-08T15:17:03Z
dc.date.issued2017-05-23
dc.identifier.citationMetaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer's disease. 2017, 114 (21):5527-5532 Proc. Natl. Acad. Sci. U.S.A.en
dc.identifier.issn1091-6490
dc.identifier.pmid28484012
dc.identifier.doi10.1073/pnas.1613700114
dc.identifier.urihttp://hdl.handle.net/10033/621198
dc.description.abstractDynamic regulation of plasticity thresholds in a neuronal population is critical for the formation of long-term plasticity and memory and is achieved by mechanisms such as metaplasticity. Metaplasticity tunes the synapses to undergo changes that are necessary prerequisites for memory storage under physiological and pathological conditions. Here we discovered that, in amyloid precursor protein (APP)/presenilin-1 (PS1) mice (age 3-4 mo), a prominent mouse model of Alzheimer's disease (AD), late long-term potentiation (LTP; L-LTP) and its associative plasticity mechanisms such as synaptic tagging and capture (STC) were impaired already in presymptomatic mice. Interestingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associative interaction of LTP and LTD, cross-capture, was altered in these mice. Metaplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC. We propose that RyR-mediated metaplastic mechanisms can be considered as a possible therapeutic target for counteracting synaptic impairments in the neuronal networks during the early progression of AD.
dc.language.isoenen
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5448214/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleMetaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer's disease.en
dc.typeArticleen
dc.contributor.departmentHelmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr.7, 38124 Braunschweig, Germany.en
dc.identifier.journalProceedings of the National Academy of Sciences of the United States of Americaen
dc.identifier.pmcidPMC5448214
refterms.dateFOA2018-06-12T21:51:45Z
html.description.abstractDynamic regulation of plasticity thresholds in a neuronal population is critical for the formation of long-term plasticity and memory and is achieved by mechanisms such as metaplasticity. Metaplasticity tunes the synapses to undergo changes that are necessary prerequisites for memory storage under physiological and pathological conditions. Here we discovered that, in amyloid precursor protein (APP)/presenilin-1 (PS1) mice (age 3-4 mo), a prominent mouse model of Alzheimer's disease (AD), late long-term potentiation (LTP; L-LTP) and its associative plasticity mechanisms such as synaptic tagging and capture (STC) were impaired already in presymptomatic mice. Interestingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associative interaction of LTP and LTD, cross-capture, was altered in these mice. Metaplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC. We propose that RyR-mediated metaplastic mechanisms can be considered as a possible therapeutic target for counteracting synaptic impairments in the neuronal networks during the early progression of AD.


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