scholarly journals Autonomic/Central Coupling Boosts Working Memory in Healthy Young Adults

2020 ◽  
Author(s):  
Pin-Chun Chen ◽  
Lauren N. Whitehurst ◽  
Mohsen Naji ◽  
Sara C. Mednick

AbstractWorking memory (WM) is an executive function that can improve with training. However, the precise mechanism for this improvement is not known. Studies have shown greater WM gains after a period of sleep than a similar period of wake (Kuriyama et al. 2008a; Zinke, Noack, and Born 2018), with WM improvement correlated with slow wave activity (SWA; 0.5-1Hz) during slow wave sleep (SWS) (Sattari et al. 2019; Pugin et al. 2015; Ferrarelli et al. 2019). A different body of literature has suggested an important role for autonomic activity during wake for WM (Hansen et al. 2004; Mosley, Laborde, and Kavanagh 2018). A recent study from our group reported that the temporal coupling of autonomic and central events (ACEs) during sleep was associated with memory consolidation (Naji et al. 2019). We found that heart rate bursts (HR bursts) during non-rapid eye movement (NREM) sleep are accompanied by increases in SWA and sigma (12-15Hz) power, as well as increases in the high-frequency (HF) component of the RR interval, reflecting vagal rebound. In addition, ACEs predict long-term, episodic memory improvement. Building on these previous results, we examined whether ACEs may also contribute to gains in WM. We tested 104 young adults in an operation span task (OSPAN) in the morning and evening, with either a nap (with electroencephalography (EEG) and electrocardiography (ECG)) or wake between testing sessions. We identified HR bursts in the ECG and replicated the increases in SWA and sigma prior to peak of the HR burst, as well as vagal rebound after the peak. Furthermore, we showed sleep-dependent WM improvement, which was predicted by ACE activity. Using regression analyses, we discovered that significantly more variance in WM improvement could be explained with ACE variables than with overall sleep activity not time-locked with ECG. These results provide the first evidence that coordinated autonomic and central events play a significant role in sleep-related WM improvement and implicate the potential of autonomic interventions during sleep for cognitive enhancement.

2020 ◽  
Vol 31 (1) ◽  
pp. 324-340
Author(s):  
Pavel Sanda ◽  
Paola Malerba ◽  
Xi Jiang ◽  
Giri P Krishnan ◽  
Jorge Gonzalez-Martinez ◽  
...  

Abstract The dialogue between cortex and hippocampus is known to be crucial for sleep-dependent memory consolidation. During slow wave sleep, memory replay depends on slow oscillation (SO) and spindles in the (neo)cortex and sharp wave-ripples (SWRs) in the hippocampus. The mechanisms underlying interaction of these rhythms are poorly understood. We examined the interaction between cortical SO and hippocampal SWRs in a model of the hippocampo–cortico–thalamic network and compared the results with human intracranial recordings during sleep. We observed that ripple occurrence peaked following the onset of an Up-state of SO and that cortical input to hippocampus was crucial to maintain this relationship. A small fraction of ripples occurred during the Down-state and controlled initiation of the next Up-state. We observed that the effect of ripple depends on its precise timing, which supports the idea that ripples occurring at different phases of SO might serve different functions, particularly in the context of encoding the new and reactivation of the old memories during memory consolidation. The study revealed complex bidirectional interaction of SWRs and SO in which early hippocampal ripples influence transitions to Up-state, while cortical Up-states control occurrence of the later ripples, which in turn influence transition to Down-state.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A34-A34
Author(s):  
E M Wernette ◽  
K M Fenn

Abstract Introduction Slow wave sleep (SWS) strengthens declarative memory for information studied for a later test. However, research on the effect of sleep on information that is not intentionally remembered is scare. Previous research from our lab suggests sleep consolidates some, but not all, information that has been encoded incidentally, meaning that it has been acted on but not intentionally remembered. It remains unclear what determines which information benefits from sleep-dependent consolidation processes and what aspects of sleep are related to these mnemonic benefits. In two experiments, we test the hypothesis that sleep consolidates strong but not weak memory traces following incidental encoding, and assess the relationship between memory performance and objective sleep characteristics. Methods In Experiment 1, participants rated words one (weak traces) or three times (strong traces) in a deep or shallow incidental encoding task. Participants either rated words on a scale from ‘concrete’ to ‘abstract’ (deep) or counted the vowels in the words (shallow). Following a 12-hour period containing sleep or wakefulness, participants took a surprise memory test. In Experiment 2, participants rated words one or three times in the deep encoding task, received an 8-hour sleep opportunity with polysomnography, and took the surprise memory test. Results In Experiment 1, participants remembered words better after sleep than wake regardless of whether words were encoded one or three times, but only after deep encoding. Sleep did not consolidate information following shallow encoding. Experiment 2 is ongoing, but we predict that the amount of SWS will correlate positively with memory. Conclusion Results thus far suggest sleep may have consolidated information based on the strength of memory traces. Because deep encoding results in stronger memory traces than shallow encoding, this work is broadly consistent with theories of memory consolidation that predict sleep is more beneficial for strong memory traces than weak, such as the synaptic downscaling hypothesis. Support N/A


2016 ◽  
Vol 34 (3_suppl) ◽  
pp. 193-193
Author(s):  
AnnaLynn Williams ◽  
Michelle Christine Janelsins ◽  
Edwin van Wijngaarden

193 Background: Cancer and its treatment may affect cognitive function in up to 35% of survivors months after treatment. While short-term treatment-related cognitive changes are well recognized, only limited research is available in older, long-term survivors of cancer. Methods: Using NHANES data from 1999 through 2002, 408 cancer survivors and 2,639 non-cancer participants age 60 and above were identified. Cognitive function of these groups were compared on self-reported problems with memory or confusion and using the Digit Symbol Substitution Test (DSST), a test of processing speed, attention, and learning and working memory involving executive functions domains. Results: Cancer survivors were on average 72.8 years old and 11.5 years from diagnosis. After adjustment for covariates, cancer survivors scored, on average, 1.99 points lower on the DSST compared to non-cancer survivors (ß=-1.99, 95%CI -3.94, -0.05). Cancer survivors also had 17% higher odds of self-reporting problems with memory or confusion (OR 1.17, 95%CI 0.89, 1.53). Similar results were observed among survivors ≥ 5 years from diagnosis (ß =-2.38, 95%CI -4.57, -0.18, OR1.41, 95%CI 0.99, 2.02). Results suggest that age modifies the association between cancer diagnosis and DSST score (p=0.11) with a larger effect size in the younger group (between 60 and 75 years). Among those younger than 75, cancer survivors performed 3.25 points lower on the DSST compared to non-cancer survivors (ß =-3.25; 95%CI -5.88, -0.62). However, this difference was only 0.18 points lower among those 75 or older (ß =-0.18; 95%CI -2.94, 2.57). Conclusions: This is the only study to examine domain specific cognitive deficits in a large, nationally representative, older population of long-term cancer survivors and the first to report deficits in processing speed, attention, and learning and working memory domains. These domains are thought to be important for social and executive functioning and quality of life. Characterizing affected domains and subpopulations will help to develop and test effective interventions and may influence treatment practices in older cancer patients.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A45-A45
Author(s):  
T Tselha ◽  
L N Whitehurst ◽  
V Tina ◽  
Y D Benjamin ◽  
S C Mednick

Abstract Introduction The goal of cognitive enhancement is to improve mental functions using interventions including cognitive training, brain stimulation and pharmacology. Indeed, psychostimulants, commonly used for cognitive enhancement purposes, while preventing sleep, have been shown to increase working memory (WM) and attention. WM is widely believed play a core role in cognitive ability, and has been shown to correlate with broad measure of cognitive ability and fluid intelligence. Sleep, however, is also important for cognitive function; thus, understanding the interaction between stimulants, sleep and cognition may inform current approaches to cognitive enhancement. Methods We used a double-blind, placebo controlled, repeated-measure design to investigate the effect of morning administration (9am) of stimulant, dextroamphetamine (DEX, 20 mg), on within-day and overnight WM performance, and sleep in 46 (22 female) healthy young adults. We tested WM using an operation span task (OSPAN) as it engages and captures both the memory retention and online processing capacity of WM. WM was tested at 75 minutes post drug, 12 h post drug, and 24 h post drug over a night of sleep. Results Compared with placebo, DEX showed no changes to WM performance at 75min or 12-hr post-drug. After sleep, DEX performed worse than PBO and the overnight improvement in performance in the PBO condition was absent in the DEX condition. Moreover, sleep quality was negatively affected by DEX administration. Conclusion In summary, we found no cognitive boost from psychostimulants across a day of wake and a blockade of overnight WM increases with the stimulant, compared to PBO. Given the growing non-medical use of stimulants in young adults, these findings have important implications for assessing their benefit for cognitive enhancement. Support Office of Naval Research N00014-14-1-0513 (S.M.) and DoD Young Investigator Prize (S.M.)


Author(s):  
Graham M. Dean ◽  
Stephen A. Dewhurst ◽  
Annalise Whittaker

Several studies have demonstrated that dynamic visual noise (DVN) does not interfere with memory for random matrices. This has led to suggestions that (a) visual working memory is distinct from imagery, and (b) visual working memory is not a gateway between sensory input and long-term storage. A comparison of the interference effects of DVN with memory for matrices and colored textures shows that DVN can interfere with visual working memory, probably at a level of visual detail not easily supported by long-term memory structures or the recoding of the visual pattern elements. The results support a gateway model of visuospatial working memory and raise questions about the most appropriate ways to measure and model the different levels of representation of information that can be held in visual working memory.


PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202198 ◽  
Author(s):  
Henning Johannes Drews ◽  
Christian Dirk Wiesner ◽  
Christina Bethke-Jaenicke ◽  
Sara Lena Weinhold ◽  
Paul Christian Baier ◽  
...  

1998 ◽  
Vol 83 (8) ◽  
pp. 2706-2710 ◽  
Author(s):  
Ralf-Michael Frieboes ◽  
Harald Murck ◽  
Günter Karl Stalla ◽  
Irina A. Antonijevic ◽  
Axel Steiger

abstract Bidirectional interactions between nocturnal hormone secretion and sleep regulation are well established. In particular, a link between PRL and rapid eye movement (REM) sleep has been hypothesized. Short-term administration of PRL and even long-term hyperprolactinemia in animals increases REM sleep. Furthermore, sleep disorders are frequent symptoms in patients with endocrine diseases. We compared the sleep electroencephalogram of seven drug-free patients with prolactinoma (mean PRL levels 1450 ± 1810 ng/mL; range between 146 and 5106 ng/mL) with that of matched controls. The patients had secondary hypogonadism but no other endocrine abnormalities. They spent more time in slow wave sleep than the controls (79.4 ± 54.4 min in patients vs. 36.6 ± 23.5 min in controls, P < 0.05). REM sleep variables did not differ between the samples. Our data suggest that chronic excessive enhancement of PRL levels exerts influences on the sleep electroencephalogram in humans. Our result, which seems to be in contrast to the enhanced REM sleep under hyperprolactinemia in rats, leads to the hypothesis that both slow wave sleep and REM sleep can be stimulated by PRL. These findings are in accordance with reports of good sleep quality in patients with prolactinoma, which is in contrast to that of patients with other endocrine diseases.


2009 ◽  
Vol 296 (1) ◽  
pp. R178-R184 ◽  
Author(s):  
Melvi M. Methippara ◽  
Tariq Bashir ◽  
Sunil Kumar ◽  
Noor Alam ◽  
Ronald Szymusiak ◽  
...  

Previous work showed that sleep is associated with increased brain protein synthesis and that arrest of protein synthesis facilitates sleep. Arrest of protein synthesis is induced during the endoplasmic reticulum (ER) stress response, through phosphorylation of eukaryotic initiation factor 2α (p-eIF2α). We tested a hypothesis that elevation of p-eIF2α would facilitate sleep. We studied the effects of intracerebroventricular infusion of salubrinal (Salub), which increases p-eIF2α by inhibiting its dephosphorylation. Salub increased deep slow wave sleep by 255%, while reducing active waking by 49%. Delta power within non-rapid eye movement (NREM) sleep was increased, while power in the sigma, beta, and gamma bands during NREM was reduced. We found that Salub increased expression of p-eIF2α in the basal forebrain (BF) area, a sleep-wake regulatory brain region. Therefore, we quantified the p-eIF2α-immunolabeled neurons in the BF area; Salub administration increased the number of p-eIF2α-expressing noncholinergic neurons in the caudal BF. In addition, Salub also increased the intensity of p-eIF2α expression in both cholinergic and noncholinergic neurons, but this was more widespread among the noncholinergic neurons. Our findings support a hypothesis that sleep is facilitated by signals associated with the ER stress response.


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