期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-05868-0
关键词
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资金
- National Institutes of Health grants [MH101491, AG051807, AG050787, T32-AG000096-31, F32-AG052303, K99-AG056596]
- NSF [IIS-1550705]
- DARPA grant [D17AP00002]
- NIH [GM123558]
- long-term EMBO post-doctoral fellowship
- ARC Foundation award
- National Institutes of Health
- INSEAM
- Novo Nordisk Foundation Challenge Program
Aging is accompanied by impairments in both circadian rhythmicity and long-term memory. Although it is clear that memory performance is affected by circadian cycling, it is unknown whether age-related disruption of the circadian clock causes impaired hippocampal memory. Here, we show that the repressive histone deacetylase HDAC3 restricts long-term memory, synaptic plasticity, and experience-induced expression of the circadian gene Per1 in the aging hippocampus without affecting rhythmic circadian activity patterns. We also demonstrate that hippocampal Per1 is critical for long-term memory formation. Together, our data challenge the traditional idea that alterations in the core circadian clock drive circadian-related changes in memory formation and instead argue for a more autonomous role for circadian clock gene function in hippocampal cells to gate the likelihood of long-term memory formation.
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