Journal
LEARNING & MEMORY
Volume 21, Issue 8, Pages 417-423Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/lm.035451.114
Keywords
-
Categories
Funding
- National Institutes of Health [NS 20498, MH 073601]
Ask authors/readers for more resources
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 Erk(1,2) 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available