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

被引：28

作者：

Middei, Silvia ^{[1
]}

Roberto, Anna ^{[1
]}

Berretta, Nicola ^{[2
]}

Panico, Maria Beatrice ^{[3
]}

Lista, Simone ^{[4
]}

Bernardi, Giorgio ^{[2
,5
]}

Mercuri, Nicola B. ^{[2
,5
]}

Ammassari-Teule, Martine ^{[1
]}

Nistico, Robert ^{[2
,6
,7
]}

机构：

[1] S Lucia Fdn, CNR, Inst Neurosci, I-00143 Rome, Italy

[2] S Lucia Fdn, Lab Expt Neurol, I-00143 Rome, Italy

[3] Univ Roma Tor Vergata, Pharmaceut Biotechnol Ctr, I-00133 Rome, Italy

[4] Neurol Fdn, Casimiro Mondino Inst, IRCCS, Lab Expt Neurobiol, I-27100 Pavia, Italy

[5] Univ Roma Tor Vergata, Dept Neurosci, I-00133 Rome, Italy

[6] Univ Calabria, Dept Pharmacobiol, I-87036 Arcavacata Di Rende, Italy

[7] Univ Calabria, UCHAD, I-87036 Arcavacata Di Rende, Italy

来源：

LEARNING & MEMORY | 2010年 / 17卷 / 05期

关键词：

AMYLOID PRECURSOR PROTEIN; LONG-TERM POTENTIATION; MILD COGNITIVE IMPAIRMENT; AGE-RELATED IMPAIRMENT; TRANSGENIC MICE; DENDRITIC SPINES; SYNAPTIC PLASTICITY; SPATIAL NAVIGATION; APICAL DENDRITES; IN-VIVO;

D O I：

10.1101/lm.1748310

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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

引用

页码：236 / 240

页数：5

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