Journal
NEUROBIOLOGY OF AGING
Volume 35, Issue 11, Pages 2474-2478Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2014.05.005
Keywords
Alzheimer's disease; Tau knock-out mice; Hippocampus; Synaptic plasticity; Long-term depression; Cognition; Morris water maze
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Funding
- FWO-Vlaanderen [G.0327.08]
- FWO junior scholarship
- IDO Project [06/004, OT 06/23]
- National institute of Health and Medical Research
- CNRS
- IMPRT
- Region Nord/Pas-de-Calais
- Fonds europeen de developpement eonomique et regional
- France Alzheimer
- Agence Nationale de la Recherche [ANR-08-MNP-002]
- European Community Programmes APOPIS (FP6) [LECMA/AFI#11701, LSHM-CT-2003-503330]
- MEM-OSAD (FP7) [2006121]
- K.U. Leuven fellowship
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Tau has been implicated in the organization, stabilization, and dynamics of microtubules. In Alzheimer's disease and more than 20 neurologic disorders tau missorting, hyperphosphorylation, and aggregation is a hallmark. They are collectively referred to as tauopathies. Although the impact of human tauopathies on cognitive processes has been explored in transgenic mouse models, the functional consequences of tau deletion on cognition are far less investigated. Here, we subjected tau knock-out ( KO) mice to a battery of neurocognitive, behavioral, and electrophysiological tests. Although KO and wild-type mice were indistinguishable in motor abilities, exploratory and anxiety behavior, KO mice showed impaired contextual and cued fear conditioning. In contrast, extensive spatial learning in the water maze resulted in better performance of KO mice during acquisition. In electrophysiological experiments, basal synaptic transmission and paired-pulse facilitation in the hippocampal CA1-region were unchanged. Interestingly, deletion of tau resulted in severe deficits in long-term potentiation but not long-term depression. Our results suggest a role of tau in certain cognitive functions and implicate long-term potentiation as the relevant physiological substrate. (C) 2014 Elsevier Inc. All rights reserved.
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