scholarly journals Contribution of adult-born neurons to memory consolidation during rapid eye movement sleep

2022 ◽  
Vol 17 (2) ◽  
pp. 307
Author(s):  
Masanori Sakaguchi ◽  
Akinobu Ohba
2020 ◽  
Vol 14 ◽  
Author(s):  
Pablo Vergara ◽  
Masanori Sakaguchi

The mammalian hippocampus generates new neurons that incorporate into existing neuronal networks throughout the lifespan, which bestows a unique form of cellular plasticity to the memory system. Recently, we found that hippocampal adult-born neurons (ABNs) that were active during learning reactivate during subsequent rapid eye movement (REM) sleep and provided causal evidence that ABN activity during REM sleep is necessary for memory consolidation. Here, we describe the potential underlying mechanisms by highlighting distinct characteristics of ABNs including decoupled firing from local oscillations and ability to undergo profound synaptic remodeling in response to experience. We further discuss whether ABNs constitute the conventional definition of engram cells by focusing on their active and passive roles in the memory system. This synthesis of evidence helps advance our thinking on the unique mechanisms by which ABNs contribute to memory consolidation.


2021 ◽  
Author(s):  
Hamid Niknazar ◽  
Sara Mednick ◽  
Paola Malerba

Slow oscillations (SOs, <1Hz) during non-rapid eye movement sleep are thought to reflect sleep homeostasis and support memory consolidation. Yet, the fundamental properties of SOs and their impact on neural network communication are not understood. We used effective connectivity to estimate causal information flow across the electrode manifold during SOs and found two peak of information flow in specific phases of the SO. We show causal communication during non-rapid eye movement sleep peaks during specific phases of the SO, but only across long distances. We confirmed this prediction by cluster analysis demonstrating greater flow in global, compared with local, SOs. Finally, we tested the functional significance of these results by examining which SO properties supported overnight episodic memory improvement, with the underlying assumption that memory consolidation would engage global, long-range communication. Indeed, episodic memory improvement was predicted only by the SO properties with greatest causal information flow, i.e., longest distances between sinks and sources and global, but not local, SOs. These findings explain how NREM sleep (characterized as a state of low brain connectivity) leverages SO-induced selective information flow to coordinate a wide network of brain regions during memory formation.


SLEEP ◽  
2019 ◽  
Vol 42 (6) ◽  
Author(s):  
Michael K Scullin ◽  
Chenlu Gao ◽  
Paul Fillmore ◽  
R Lynae Roberts ◽  
Natalya Pruett ◽  
...  

2019 ◽  
Author(s):  
Sarah K. Schäfer ◽  
Benedikt E. Wirth ◽  
Marlene Staginnus ◽  
Nicolas Becker ◽  
Tanja Michael ◽  
...  

SummaryNumerous studies have shown that sleep enhances the consolidation of episodic memory. However, it remains unclear whether this consolidation benefit is moderated by the emotional valence of the learned material. To clarify whether sleep selectively enhances the consolidation of emotional material, we conducted a meta-analysis including N = 1,059 observations. Overall, our results do not support this hypothesis. When only studies with a sleep-group wake-group comparison were included in the analysis (k = 22), the retention advantage for emotional over neutral material was not significantly different between sleep and wake groups. When studies initially lacking a wake-control group were included in the analysis after statistical estimation of wake-group parameters, the retention advantage for emotional material was significantly larger in wake-groups than in sleep-groups (k = 34). Interestingly, however, an additional analysis of k = 8 studies investigating the selective effects of rapid-eye-movement sleep and slow-wave sleep on emotional memory consolidation provided evidence for a selective enhancement of emotional over neutral memory consolidation after rapid-eye-movement sleep compared to slow-wave sleep. These results suggest that sleep does not generally enhance emotional memory consolidation over neutral memory consolidation. However, specific sleep stages might preferentially enhance consolidation of emotional and neutral material, respectively.


SLEEP ◽  
2022 ◽  
Author(s):  
Dimitrios Mylonas ◽  
Sasha Machado ◽  
Olivia Larson ◽  
Rudra Patel ◽  
Roy Cox ◽  
...  

Abstract Study Objectives Converging evidence from neuroimaging, sleep, and genetic studies suggests that dysregulation of thalamocortical interactions mediated by the thalamic reticular nucleus (TRN) contribute to autism spectrum disorder (ASD). Sleep spindles assay TRN function, and their coordination with cortical slow oscillations (SOs) indexes thalamocortical communication. These oscillations mediate memory consolidation during sleep. In the present study, we comprehensively characterized spindles and their coordination with SOs in relation to memory and age in children with ASD. Methods Nineteen children and adolescents with ASD, without intellectual disability, and 18 typically developing (TD) peers, aged 9-17, completed a home polysomnography study with testing on a spatial memory task before and after sleep. Spindles, SOs, and their coordination were characterized during stages 2 (N2) and 3 (N3) non-rapid eye movement sleep. Results ASD participants showed disrupted SO-spindle coordination during N2 sleep. Spindles peaked later in SO upstates and their timing was less consistent. They also showed a spindle density (#/min) deficit during N3 sleep. Both groups showed significant sleep-dependent memory consolidation, but its relations with spindle density differed. While TD participants showed the expected positive correlations, ASD participants showed the opposite. Conclusions The disrupted SO-spindle coordination and spindle deficit provide further evidence of abnormal thalamocortical interactions and TRN dysfunction in ASD. The inverse relations of spindle density with memory suggest a different function for spindles in ASD than TD. We propose that abnormal sleep oscillations reflect genetically mediated disruptions of TRN-dependent thalamocortical circuit development that contribute to the manifestations of ASD and are potentially treatable.


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