Journal
NEURON
Volume 110, Issue 23, Pages 4000-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2022.09.004
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Funding
- National Key R&D Program of China [2021YFA0805000, 2018YFA0109600]
- National Natural Science Foundation of China [31925018, 32127801, 31921003, 61890952]
- Chongqing Basic Research [cstc2019jcyjjqX0001]
- Guangxi Science and Technology Base and Talents Fund [GUIKE AD22035948]
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The hippocampal CA2 region is crucial for social memory, and sleep plays a vital role in the consolidation of social memory. Research has shown that hypothalamic neurons projecting to CA2 are highly active during REM sleep and silencing these neurons disrupts social memory consolidation.
The hippocampal CA2 region plays a key role in social memory. The encoding of such memory involves afferent activity from the hypothalamic supramammillary nucleus (SuM) to CA2. However, the neuronal cir-cuits required for consolidation of freshly encoded social memory remain unknown. Here, we used circuit -specific optical and single-cell electrophysiological recordings in mice to explore the role of sleep in social memory consolidation and its underlying circuit mechanism. We found that SuM neurons projecting to CA2 were highly active during rapid-eye-movement (REM) sleep but not during non-REM sleep or quiet wake-fulness. REM-sleep-selective optogenetic silencing of these neurons impaired social memory. By contrast, the silencing of another group of REM sleep-active SuM neurons that projects to the dentate gyrus had no effect on social memory. Therefore, we provide causal evidence that the REM sleep-active hypothalamic neurons that project to CA2 are specifically required for the consolidation of social memory.
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