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Abstract
Perturbing the circadian system by electrolytically lesioning the suprachiasmatic nucleus (SCN) or varying the environmental light:dark schedule impairs memory, suggesting that memory depends on the circadian system. We used a genetic approach to evaluate the role of the molecular clock in memory. Bmal1−/− mice, which are arrhythmic under constant conditions, were examined for hippocampus-dependent memory, LTP at the Schaffer-collateral synapse, and signal transduction activity in the hippocampus. Bmal1−/− mice exhibit impaired contextual fear and spatial memory. Furthermore, LTP in hippocampal slices from Bmal1−/− mice is also significantly decreased relative to that from wild-type mice. Activation of Erk1,2 MAP kinase (MAPK) during training for contextual fear memory and diurnal oscillation of MAPK activity and cAMP in the hippocampus is also lost in Bmal1−/− mice, suggesting that the memory defects are due to reduction of the memory consolidation pathway in the hippocampus. We conclude that critical signaling events in the hippocampus required for memory depend on BMAL1.
Department
Molecular, Cellular and Biomedical Sciences
Publication Date
8-1-2014
Journal Title
Learning & Memory
Publisher
Cold Spring Harbor Laboratory Press
Digital Object Identifier (DOI)
Document Type
Article
Recommended Citation
Wardlaw SM, Phan TX, Saraf A, Chen X, Storm DR. Genetic disruption of the core circadian clock impairs hippocampus-dependent memory. Learning & memory. 2014;21(8):417-23. doi: 10.1101/lm.035451.114. PubMed PMID: 25034823; PubMed Central PMCID: PMC4105720.
Rights
© 2014 Wardlaw et al.
Comments
This is an article published by Cold Spring Harbor Laboratory Press in Learning & Memory in 2014, available online: https://dx.doi.org/10.1101/lm.035451.114