rapid eye movement sleep
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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.


Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 17
Author(s):  
Mayumi Machida ◽  
Brook L. W. Sweeten ◽  
Austin M. Adkins ◽  
Laurie L. Wellman ◽  
Larry D. Sanford

The basolateral amygdala (BLA) mediates the effects of stress and fear on rapid eye movement sleep (REM) and on REM-related theta (θ) oscillatory activity in the electroencephalograph (EEG), which is implicated in fear memory consolidation. We used optogenetics to assess the potential role of BLA glutamate neurons (BLAGlu) in regulating behavioral, stress and sleep indices of fear memory, and their relationship to altered θ. An excitatory optogenetic construct targeting glutamatergic cells (AAV-CaMKIIα-hChR2-eYFP) was injected into the BLA of mice. Telemetry was used for real-time monitoring of EEG, activity, and body temperature to determine sleep states and stress-induced hyperthermia (SIH). For 3 h following shock training (ST: 20 footshocks, 0.5 mA, 0.5 s, 1 min interval), BLA was optogenetically stimulated only during REM (REM + L) or NREM (NREM + L). Mice were then re-exposed to the fear context at 24 h, 48 h, and 1 week after ST and assessed for behavior, SIH, sleep and θ activity. Control mice were infected with a construct without ChR2 (eYFP) and studied under the same conditions. REM + L significantly reduced freezing and facilitated immediate recovery of REM tested at 24 h and 48 h post-ST during contextual re-exposures, whereas NREM + L had no significant effect. REM + L significantly reduced post-ST REM-θ, but attenuated REM-θ reductions at 24 h compared to those found in NREM + L and control mice. Fear-conditioned SIH persisted regardless of treatment. The results demonstrate that BLAGlu activity during post-ST REM mediates the integration of behavioral and sleep indices of fear memory by processes that are associated with θ oscillations within the amygdalo-hippocampal pathway. They also demonstrate that fear memories can remain stressful (as indicated by SIH) even when fear conditioned behavior (freezing) and changes in sleep are attenuated.


2021 ◽  
Vol 12 ◽  
Author(s):  
Risto Halonen ◽  
Liisa Kuula ◽  
Tommi Makkonen ◽  
Jaakko Kauramäki ◽  
Anu-Katriina Pesonen

The neurophysiological properties of rapid eye movement sleep (REMS) are believed to tune down stressor-related emotional responses. While prior experimental findings are controversial, evidence suggests that affective habituation is hindered if REMS is fragmented. To elucidate the topic, we evoked self-conscious negative affect in the participants (N = 32) by exposing them to their own out-of-tune singing in the evening. Affective response to the stressor was measured with skin conductance response and subjectively reported embarrassment. To address possible inter-individual variance toward the stressor, we measured the shame-proneness of participants with an established questionnaire. The stressor was paired with a sound cue to pilot a targeted memory reactivation (TMR) protocol during the subsequent night's sleep. The sample was divided into three conditions: control (no TMR), TMR during slow-wave sleep, and TMR during REMS. We found that pre- to post-sleep change in affective response was not influenced by TMR. However, REMS percentage was associated negatively with overnight skin conductance response habituation, especially in those individuals whose REMS was fragmented. Moreover, shame-proneness interacted with REM fragmentation such that the higher the shame-proneness, the more the affective habituation was dependent on non-fragmented REMS. In summary, the potential of REMS in affective processing may depend on the quality of REMS as well as on individual vulnerability toward the stressor type.


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