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Let sleeping mice remember

The role of REM (rapid eye movement) sleep for memory consolidation has been discussed for a long time. Boyce et al. used optogenetics to inhibit theta oscillations in the mouse hippocampus during REM sleep (see the Perspective by Kocsis). Both object recognition memory and contextual fear memory were impaired. This consolidation mechanism occurred in a critical time window immediately after training. Disrupting the same system for similar durations during non-REM sleep or wakefulness had no effect on memory.
Science, this issue p. 812; see also p. 770

Abstract

Rapid eye movement sleep (REMS) has been linked with spatial and emotional memory consolidation. However, establishing direct causality between neural activity during REMS and memory consolidation has proven difficult because of the transient nature of REMS and significant caveats associated with REMS deprivation techniques. In mice, we optogenetically silenced medial septum γ-aminobutyric acid–releasing (MSGABA) neurons, allowing for temporally precise attenuation of the memory-associated theta rhythm during REMS without disturbing sleeping behavior. REMS-specific optogenetic silencing of MSGABA neurons selectively during a REMS critical window after learning erased subsequent novel object place recognition and impaired fear-conditioned contextual memory. Silencing MSGABA neurons for similar durations outside REMS episodes had no effect on memory. These results demonstrate that MSGABA neuronal activity specifically during REMS is required for normal memory consolidation.
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Figs. S1 to S8
Tables S1 to S9
References (2427)

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Information & Authors

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Published In

Science
Volume 352Issue 628713 May 2016
Pages: 812 - 816

History

Received: 9 October 2015
Accepted: 24 March 2016

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Authors

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Richard Boyce
Integrated Program in Neuroscience, McGill University, Montreal, Quebec, Canada.
Stephen D. Glasgow
Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
Sylvain Williams*, [email protected]
Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
Antoine Adamantidis*, [email protected]
Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
Department of Neurology and Department of Clinical Research, Inselspital University Hospital, University of Bern, Bern, Switzerland.

Notes

*Corresponding author. Email: [email protected] (S.W.); [email protected] (A.A.)
These authors contributed equally to this work.

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Science
Volume 352|Issue 6287
13 May 2016
Submission history
Received:9 October 2015
Accepted:24 March 2016
Published in print:13 May 2016
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