https://dx.doi.org/10.1101/lm.035451.114">
 

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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.

Publication Date

8-1-2014

Journal Title

Learning & Memory

Publisher

Cold Spring Harbor Laboratory Press

Digital Object Identifier (DOI)

https://dx.doi.org/10.1101/lm.035451.114

Document Type

Article

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

Share

COinS