Learning discloses abnormal structural and functional plasticity in hippocampal synapses of the APP23 mouse model of Alzheimer Disease

Abstract

Event Abstract Back to Event Learning discloses abnormal structural and functional plasticity in hippocampal synapses of the APP23 mouse model of Alzheimer Disease Silvia Middei1*, Robert Nistico2, Anna Roberto1, Nicola Berretta1, Nicola Mercuri3, 4 and Martine Ammassari-Teule1 1 S. Lucia Foundation, CNR Institute of Neuroscience, Italy 2 University of Calabria, Department of Pharmacobiology, Italy 3 S. Lucia Foundation, Department of Experimental Neurology, Italy 4 University of Tor Vergata, Department of Neuroscience, Faculty of Health,Medicine and Life Sciences, Italy Transgenic mouse models generated for Alzheimer’s Disease (AD) showing histological hallmarks of the pathology do not present, in some cases, major abnormalities in cognitive abilities or synaptic plasticity. For instance, APP23 mice overexpressing human APP with AD-linked mutations develop characteristic pathologies but still display normal hippocampal Long Term Potentiation and sligth learning abilities. Negative findings migth be due to insufficient challenge of APP23 mice learning capabilities, raising in turn the possibility that the absence of mutation effects on baseline plasticity does not necessarily mean that plasticity is intact at the time it comes into play. To test this hypothesis, we investigated modifications in dendritic spine parameters, synaptic transmission and LTP in CA1 hippocampal synapses of the APP23 mice in relation to their previous exposition to a spatial learning task. We found that a slight cognitive impairment in Morris Water Maze task is accompanied by dendritic spines subtle alteration in the CA1 region of the hippocampus of APP23 mice. As a consequence of learning, spines modifications in number and size occurs both in wild type and APP23 mice, although with different modalities. Also, spatial training unmasks a deficit in LTP expression at CA1 synapses of APP23 but not of control mice. Overall, we demonstrate that hippocampal structural and functional deficits in synaptic plasticity clearly emerge in APP23 mice only when previously challenged by a learning experience. These experimental results are in line with the common clinical evidence that mild cognitive alterations typically associated to the prodromic stage of AD are evident in relation to the difficulty of the behavioral challenge faced. Moreover, our data may have critical implications for the use of AD animal models, in particular for the correct evaluation of the progress of the disease in relation to histological markers, cognitive impaiment and synaptic alterations. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Poster Presentation Topic: Poster presentations Citation: Middei S, Nistico R, Roberto A, Berretta N, Mercuri N and Ammassari-Teule M (2009). Learning discloses abnormal structural and functional plasticity in hippocampal synapses of the APP23 mouse model of Alzheimer Disease. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.234 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Jun 2009; Published Online: 11 Jun 2009. * Correspondence: Silvia Middei, S. Lucia Foundation, CNR Institute of Neuroscience, Rome, Italy, s.middei@hsantalucia.it Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Silvia Middei Robert Nistico Anna Roberto Nicola Berretta Nicola Mercuri Martine Ammassari-Teule Google Silvia Middei Robert Nistico Anna Roberto Nicola Berretta Nicola Mercuri Martine Ammassari-Teule Google Scholar Silvia Middei Robert Nistico Anna Roberto Nicola Berretta Nicola Mercuri Martine Ammassari-Teule PubMed Silvia Middei Robert Nistico Anna Roberto Nicola Berretta Nicola Mercuri Martine Ammassari-Teule Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.