Journal
JOURNAL OF NEUROSCIENCE
Volume 32, Issue 23, Pages 8004-8011Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5369-11.2012
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Funding
- NIH [K08 NS069811, R01 EY018742, DP2 OD006662]
- Dr. and Mrs. E.P. Richardson Jr. Fund for Neuropathology
- Ludcke Foundation
- Pierce Charitable Trust
- Mathers Charitable Foundation
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Amyloid-beta (A beta)-induced changes in synaptic function in experimental models of Alzheimer's disease ( AD) suggest that A beta generation and accumulation may affect fundamental mechanisms of synaptic plasticity. To test this hypothesis, we examined the effect of APP overexpression on a well characterized, in vivo, developmental model of systems-level plasticity, ocular dominance plasticity. Following monocular visual deprivation during the critical period, mice that express mutant alleles of amyloid precursor protein (APPswe) and Presenilin1 (PS1dE9), as well as mice that express APPswe alone, lack ocular dominance plasticity in visual cortex. Defects in the spatial extent and magnitude of the plastic response are evident using two complementary approaches, Arc induction and optical imaging of intrinsic signals in awake mice. This defect in a classic paradigm of systems level synaptic plasticity shows that A beta overexpression, even early in postnatal life, can perturb plasticity in cerebral cortex, and supports the idea that decreased synaptic plasticity due to elevated A beta exposure contributes to cognitive impairment in AD.
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