http://www.cnr.it/ontology/cnr/individuo/prodotto/ID38727
Learning discloses abnormal structural and functional plasticity at hippocampal synapses in the APP23 mouse model of Alzheimer's disease. (Articolo in rivista)
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- Learning discloses abnormal structural and functional plasticity at hippocampal synapses in the APP23 mouse model of Alzheimer's disease. (Articolo in rivista) (literal)
- Anno
- 2010-01-01T00:00:00+01:00 (literal)
- Alternative label
Middei S, Roberto A, Berretta N, Panico MB, Lista S, Bernardi G, Mercuri NB, Ammassari-Teule M, Nisticò R. (2010)
Learning discloses abnormal structural and functional plasticity at hippocampal synapses in the APP23 mouse model of Alzheimer's disease.
in Learning & memory (Cold Spring Harbor N.Y. Online)
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- Middei S, Roberto A, Berretta N, Panico MB, Lista S, Bernardi G, Mercuri NB, Ammassari-Teule M, Nisticò R. (literal)
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- ISI Web of Science (WOS) (literal)
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- Istituto di neuroscienze (literal)
- Titolo
- Learning discloses abnormal structural and functional plasticity at hippocampal synapses in the APP23 mouse model of Alzheimer's disease. (literal)
- Abstract
- B6-Tg/Thy1APP23Sdz (APP23) mutant mice exhibit neurohistological hallmarks of Alzheimer's disease but show intact
basal hippocampal neurotransmission and synaptic plasticity. Here, we examine whether spatial learning differently modifies
the structural and electrophysiological properties of hippocampal synapses in APP23 and wild-type mice. While no
genotypic difference was found in the pseudotrained mice, training elicited a stronger increase in spine density and a
more rapid decay of long-term potentiation (LTP) in APP23 mutants. Thus, learning discloses mutation-related abnormalities
regarding dendritic spine formation and LTP persistence, thereby suggesting that although unaltered in naI¨ve synapses,
plasticity becomes defective at the time it comes into play. (literal)
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