scholarly journals 0115 Do Theta Power and other Baseline REM Sleep Parameters Predict Fear Conditioning, Extinction, and Extinction Recall in Healthy Adults?

SLEEP ◽  
2018 ◽  
Vol 41 (suppl_1) ◽  
pp. A45-A45
Author(s):  
A Germain ◽  
G Lynch ◽  
H Khan ◽  
R McNamee ◽  
C Oh ◽  
...  
2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A62-A62
Author(s):  
M Schenker ◽  
L Ney ◽  
L Miller ◽  
K Felmingham ◽  
C Nicholas ◽  
...  

Abstract Sleep may contribute to the long-lasting consolidation and processing of emotional memories. Experimental fear conditioning and extinction paradigms model the development, maintenance, and treatment of anxiety disorders. The literature provides compelling evidence for the involvement of rapid eye movement (REM) sleep in the consolidation of such memories. This meta-analysis correlated polysomnographic sleep findings with psychophysiological reactivity to the danger (CS+) and safety stimuli (CS-), to clarify the specific role of sleep stages before and after fear conditioning, extinction learning and extinction recall. Overall, there was evidence that more pre-learning sleep stage two and less slow wave sleep was associated with higher psychophysiological reactivity to the safety stimulus during extinction learning. Preliminary evidence found here support the role of REM sleep during the post-extinction consolidation sleep phase in clinical populations with disrupted sleep, but not in healthy controls. Furthermore, the meta-regressions found that sex moderated the associations between sleep and psychophysiological reactivity throughout the paradigm providing evidence for diverging correlations in male and females. Specifically, increased post-extinction REM was associated with poorer extinction and safety recall in females while the opposite was found in males. These results have implications for future research in the role of sleep in emotional memory processing.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A236-A237
Author(s):  
Jodi Gustave ◽  
Kaelyn Gaza ◽  
Jennifer Marriner ◽  
Seema Rani ◽  
Abigail Strang ◽  
...  

Abstract Introduction Children with achondroplasia and Trisomy 21 (T21) have increased incidence of sleep disturbances including sleep disordered breathing. Abnormal sleep architecture has been documented in children with T21. It is important to continue to analyze sleep parameters in both groups since poor sleep quality is associated with neurocognitive impairment. Methods Following IRB approval, we performed a retrospective chart review of patients at Nemours/A.I. duPont Hospital for Children in Wilmington, DE with achondroplasia and T21 who underwent an initial polysomnogram (PSG) between 2015 and 2020. We compared sleep architecture parameters between the groups including sleep efficiency, total sleep time (TST), sleep latency, arousal index and concentration of N3 and REM sleep. Results In patients with achondroplasia (n=49, mean age 5.8 months and 63.3% male), 12% reported restless sleep. PSG data revealed TST of 392 minutes, mean sleep efficiency of 82%, mean sleep latency of 9.4 min, mean arousal index of 40, 22% REM sleep and 32% N3 sleep. In the patients with T21 (n=32, mean age 17.8 months and 50% male), 59% reported restless sleep. PSG data revealed TST of 393 minutes, mean sleep efficiency of 82%, mean sleep latency of 14 minutes, arousal index of 35, 15% REM sleep and 40% N3 sleep. The differences in REM and N3 sleep between the two groups were statistically significant (p-values of 0.001 and 0.04, respectively), but the differences in arousal index, TST and sleep efficiency were not. Conclusion Our study showed that children with T21 subjectively noted more restless sleep compared to patients with achondroplasia although TST and sleep efficiency were similar. Patients with achondroplasia had a higher arousal index that was not statistically significant. Children with achondroplasia had a shorter sleep latency and more robust REM concentration, likely due to their younger age. There was a higher concentration of N3 sleep in patients with T21. This is likely due to the decrease in REM concentration. In conclusion, it is important to establish expected sleep parameters in patients with achondroplasia and T21 to maximize sleep quality and mitigate negative neurocognitive effects of poor sleep. Support (if any):


2010 ◽  
Vol 203 (2) ◽  
pp. 285-297 ◽  
Author(s):  
Erin L. Zelinski ◽  
Nancy S. Hong ◽  
Amanda V. Tyndall ◽  
Brett Halsall ◽  
Robert J. McDonald

1989 ◽  
Vol 72 (2) ◽  
pp. 118-125 ◽  
Author(s):  
Cindy L. Ehlers ◽  
David J. Kupfer
Keyword(s):  

2015 ◽  
Vol 57 (7) ◽  
pp. 818-832 ◽  
Author(s):  
Miriam Liora Den ◽  
Bronwyn M. Graham ◽  
Carol Newall ◽  
Rick Richardson

2019 ◽  
Author(s):  
Francesca Billwiller ◽  
Laura Castillo ◽  
Heba Elseedy ◽  
Anton Ivanovich Ivanov ◽  
Jennyfer Scapula ◽  
...  

AbstractSeveral studies suggest that neurons from the lateral region of the SuM (SuML) innervating the dorsal dentate gyrus (DG) display a dual GABAergic and glutamatergic transmission and are specifically activated during paradoxical (REM) sleep (PS). The objective of the present study is to fully characterize the anatomical, neurochemical and electrophysiological properties of the SuML-DG projection neurons and to determine how they control DG oscillations and neuronal activation during PS and other vigilance states. For this purpose, we combine structural connectivity techniques using neurotropic viral vectors (rabies virus, AAV), neurochemical anatomy (immunohistochemistry, in situ hybridization) and imaging (light, electron and confocal microscopy) with in vitro (patch clamp) and in vivo (LFP, EEG) optogenetic and electrophysiological recordings performed in transgenic VGLUT2-cre male mice. At the cellular level, we show that the SuML-DG neurons co-release GABA and glutamate on dentate granule cells and increase the activity of a subset of DG granule cells. At the network level, we show that activation of the SuML-DG pathway increases theta power and frequency during PS as well as gamma power during PS and waking in the DG. At the behavioral level, we show that the activation of this pathway does not change animal behavior during PS, induces awakening during slow wave sleep and increases motor activity during waking. These results suggest that the SuML-DG pathway is capable of supporting the increase of theta and gamma power in the DG observed during PS and plays an important modulatory role of DG network activity during this state.Significant statementAn increase of theta and gamma power in the dentate gyrus (DG) is an hallmark of paradoxical (REM) sleep (PS) and is suggested to promote learning and memory consolidation by synchronizing hippocampal networks and increasing its outputs to cortical targets. However the neuronal networks involved in such control of DG activity during PS are poorly understood. The present study identifies a population of GABA/Glutamate neurons in the lateral supramammllary nucleus (SuML) innervating the DG that could support such control during PS. Indeed, we show that activation of these SuML-DG projections increase theta power and frequency as well as gamma power in the DG specifically during PS and modulate activity of a subset of DG granule cells.


2020 ◽  
Vol 11 ◽  
Author(s):  
Hanul Lee ◽  
Hyunjin Cho ◽  
Yeong Sim Choe ◽  
Sang Won Seo ◽  
Eun Yeon Joo

Background and Objectives: Amyloid-beta protein may lead to sleep disturbance and eventually develop cognitive impairment. Idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) is a predictor of neurodegeneration, yet there have been limited studies evaluating the relationship between cognitive decline and amyloid accumulation in iRBD patients. The aim of this study is to investigate the clinical and sleep characteristics of iRBD patients and its association with amyloid deposition.Methods: We enroll 23 iRBD patients (mean age, 65.8 years; male, 73.9%), and their mean history of clinically suspected RBD was 6.5 years. All underwent 18F-flutemetamol amyloid PET completed polysomnography (PSG) and questionnaires. Patients were classified into two groups according to amyloid deposition as amyloid positive and negative. Clinical and sleep parameters were compared between groups and were correlated with amyloid deposition, calculated as a standardized uptake value ratio (SUVR).Results: Four patients (17.4%) were revealed to be amyloid positive, and they showed increased percentage of wake after sleep onset (WASO), stage N1, and stage N2 sleep and worse on the Stroop Word Color Test compared to amyloid negative patients. Global SUVR was correlated with total sleep time, sleep efficiency, WASO, and N1 sleep, and these sleep parameters were associated with a part of default mode network of brains such as orbitofrontal, dorsolateral pre-frontal, and left temporal areas.Conclusion: iRBD patients with amyloid deposition have worse sleep quality than patients without amyloid. Relationship between fragmented sleep and amyloid deposition in the default mode network may be crucial to elucidate the disease progress of iRBD.


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