Synaptic Plasticity Defect Following Visual Deprivation in Alzheimer's Disease Model Transgenic Mice
| Autor: | Christopher William, Carla J. Shatz, Bradley T. Hyman, Mark W. Albers, Mark L. Andermann, R. C. Reid, Glenn J. Goldey, Demetris K. Roumis, Matthew P. Frosch |
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| Rok vydání: | 2012 |
| Předmět: |
Mice
Transgenic Polymerase Chain Reaction Eye Enucleation Fluorescence Article Amyloid beta-Protein Precursor Mice Alzheimer Disease Neuroplasticity Image Processing Computer-Assisted Presenilin-1 Amyloid precursor protein medicine Animals Humans RNA Messenger In Situ Hybridization Vision Ocular Visual Cortex Neurons Neuronal Plasticity Arc (protein) biology General Neuroscience medicine.disease Immunohistochemistry Mice Inbred C57BL Synaptic fatigue medicine.anatomical_structure Cerebral cortex Synapses Synaptic plasticity biology.protein Developmental plasticity Sensory Deprivation Alzheimer's disease Neuroscience Photic Stimulation |
| Zdroj: | Journal of Neuroscience. 32:8004-8011 |
| ISSN: | 1529-2401 0270-6474 |
| Popis: | Amyloid-beta (Aβ)-induced changes in synaptic function in experimental models of Alzheimer disease (AD) suggest that Aβ generation and accumulation may affect fundamental mechanisms of synaptic plasticity. To test this hypothesis, we examined the effect of amyloid precursor protein (APP) overexpression on a well-characterized, in vivo, developmental model of systems-level plasticity, ocular dominance plasticity (ODP). 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 Aβ overexpression, even early in postnatal life, can perturb plasticity in cerebral cortex, and supports the idea that decreased synaptic plasticity due to elevated Aβ exposure contributes to cognitive impairment in AD. |
| Databáze: | OpenAIRE |
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