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Impairments in experience‐dependent scaling and stability of hippocampal place fields limit spatial learning in a mouse model of Alzheimer's disease
Author(s) -
Zhao Rong,
Fowler Stephanie W.,
Chiang Angie C.A.,
Ji Daoyun,
Jankowsky Joanna L.
Publication year - 2014
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.22283
Subject(s) - hippocampal formation , neuroscience , water maze , psychology , morris water navigation task , hippocampus , alzheimer's disease , spatial memory , recall , spatial learning , environmental enrichment , place cell , cognition , disease , working memory , cognitive psychology , medicine
Impaired spatial memory characterizes many mouse models for Alzheimer's disease, but we understand little about how this trait arises. Here, we use a transgenic model of amyloidosis to examine the relationship between behavioral performance in tests of spatial navigation and the function of hippocampal place cells. We find that amyloid precursor protein (APP) mice require considerably more training than controls to reach the same level of performance in a water maze task, and recall the trained location less well 24 h later. At a single cell level, place fields from control mice become more stable and spatially restricted with repeated exposure to a new environment, while those in APP mice improve less over time, ultimately producing a spatial code of lower resolution, accuracy, and reliability than controls. The limited refinement of place fields in APP mice likely contributes to their delayed water maze acquisition, and provides evidence for circuit dysfunction underlying cognitive impairment. © 2014 Wiley Periodicals, Inc.