Learning discloses abnormal structural and functional plasticity at hippocampal synapses in the APP23 mouse model of Alzheimer's disease

Silvia Middei, Anna Roberto, Nicola Berretta, Maria Beatrice Panico, Simone Lista, Giorgio Bernardi, Nicola B. Mercuri, Martine Ammassari-Teule, Robert Nisticò

Research output: Contribution to journalArticle

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 naïve synapses, plasticity becomes defective at the time it comes into play.

Original languageEnglish
Pages (from-to)236-240
Number of pages5
JournalLearning and Memory
Volume17
Issue number5
DOIs
Publication statusPublished - May 2010

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cognitive Neuroscience
  • Neuropsychology and Physiological Psychology

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