Metaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer's disease.
Name:
Li et al.pdf
Size:
1.022Mb
Format:
PDF
Description:
free text from BioMed Centrals ...
Average rating
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Star rating
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Issue Date
2017-05-23
Metadata
Show full item recordAbstract
Dynamic 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.Citation
Metaplasticity 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.Affiliation
Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr.7, 38124 Braunschweig, Germany.PubMed ID
28484012PubMed Central ID
PMC5448214Additional Links
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5448214/Type
ArticleLanguage
enISSN
1091-6490ae974a485f413a2113503eed53cd6c53
10.1073/pnas.1613700114
Scopus Count
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
Related articles
- Making synapses strong: metaplasticity prolongs associativity of long-term memory by switching synaptic tag mechanisms.
- Authors: Li Q, Rothkegel M, Xiao ZC, Abraham WC, Korte M, Sajikumar S
- Issue date: 2014 Feb
- Nitric oxide signaling is recruited as a compensatory mechanism for sustaining synaptic plasticity in Alzheimer's disease mice.
- Authors: Chakroborty S, Kim J, Schneider C, West AR, Stutzmann GE
- Issue date: 2015 Apr 29
- Calcium signaling, excitability, and synaptic plasticity defects in a mouse model of Alzheimer's disease.
- Authors: Zhang H, Liu J, Sun S, Pchitskaya E, Popugaeva E, Bezprozvanny I
- Issue date: 2015
- Defective Age-Dependent Metaplasticity in a Mouse Model of Alzheimer's Disease.
- Authors: Megill A, Tran T, Eldred K, Lee NJ, Wong PC, Hoe HS, Kirkwood A, Lee HK
- Issue date: 2015 Aug 12
- Colivelin Ameliorates Impairments in Cognitive Behaviors and Synaptic Plasticity in APP/PS1 Transgenic Mice.
- Authors: Wu M, Shi H, He Y, Yuan L, Qu X, Zhang J, Wang Z, Cai H, Qi J
- Issue date: 2017