New research reveals how sleep deprivation impairs the brain's ability to suppress unwanted memories, highlighting the critical role of REM sleep.
Study: Memory control deficits in the sleep-deprived human brain. Image Credit: l i g h t p o e t/Shutterstock.com
In a recent study published in the Psychological and Cognitive Sciences, a group of researchers investigated how sleep deprivation impairs memory inhibitory control and contributes to intrusive memories, focusing on the role of Rapid Eye Movement (REM) sleep in restoring this function.
Background
Intrusive memories of unpleasant experiences can significantly impact mental health, especially in conditions like depression, anxiety, and posttraumatic stress disorder. Suppressing these memories helps weaken their impact, reducing future intrusions and aiding emotional regulation.
This process depends on effective cognitive control, mediated by brain regions such as the right dorsolateral prefrontal cortex (rDLPFC), which suppresses hippocampal memory retrieval.
Sleep, particularly REM sleep, is crucial in restoring this mechanism, yet its precise role remains unclear. Further research is essential to clarify how disrupted sleep impacts neural and cognitive processes underpinning memory suppression and its broader effects on emotional well-being.
About the study
Eighty-seven healthy adults aged 18 to 30 participated in a study examining the effects of sleep deprivation on memory suppression. Participants were right-handed, native English speakers with no history of neurological, psychiatric, or sleep disorders.
They reported regular waking hours by 8:00 AM and at least six hours of sleep per night. Written informed consent was obtained from all participants, and they were compensated with £80 or academic credit.
Two participants were excluded for not adhering to the study protocol, leaving a final sample of 85. Participants were randomly assigned to either a sleep-deprivation group (n = 43) or a restful sleep group (n = 42).
Participants completed cognitive and affective tasks across two sessions—one in the evening and one the following morning. The sleep-deprived group remained awake under supervision, while the rested group had an eight-hour sleep opportunity monitored by polysomnography (PSG). Compliance with the protocol was confirmed using actigraphy wristwatches.
Tasks included memory encoding and suppression exercises, magnetic resonance imaging (MRI) scans, and affective ratings. Functional MRI (fMRI) assessed brain activity, while behavioral analyses revealed impaired memory suppression in the sleep-deprived group, with higher intrusion rates compared to the rested group.
These results highlight the crucial role of sleep, particularly REM sleep, in enabling effective memory control.
Study results
Sleep deprivation significantly impairs the brain's ability to suppress intrusive memories. Following a night of sleep deprivation (n = 43, mean age 19.58 years) or restful sleep (n = 42, mean age 20.33 years), participants performed the Think/No-Think (TNT) task while undergoing fMRI. In this task, participants either actively retrieved or suppressed memories associated with visual cues.
We tracked suppression attempts that failed and led to memory intrusions. Behavioral analyses revealed that while suppression reduced intrusions over time for all participants, sleep-deprived individuals showed a slower reduction, reflecting impaired adaptive memory suppression.
Interestingly, this impairment was not influenced by the emotional valence of the memories. However, baseline differences in memory control ability between groups partially explained these findings.
Sleep-deprived participants performed better during preliminary tasks before the overnight interval, which may have influenced subsequent results.
Nonetheless, by the final trial blocks, the difference in intrusion rates between groups disappeared, suggesting that sleep deprivation primarily hinders the improvement of suppression over time rather than overall suppression ability.
Heart rate variability (HRV), particularly the high-frequency component (HF-HRV), was examined to explore physiological correlates of memory control. In the sleep-rested group, higher HF-HRV was linked to better suppression, while in sleep-deprived individuals, higher HF-HRV unexpectedly correlated with poorer suppression, suggesting that the benefits of HF-HRV are contingent on sufficient sleep.
Neuroimaging data further highlighted the impact of sleep deprivation. The rDLPFC, a region crucial for memory suppression, showed reduced activation in the sleep-deprived group.
Concurrently, the right hippocampus, typically deactivated during suppression, displayed diminished disengagement, indicating disrupted memory control circuits. Whole-brain analyses confirmed these findings, with reduced prefrontal control and increased hippocampal activity after sleep deprivation.
REM sleep was found to play a restorative role. In the restful sleep group, longer REM sleep duration was associated with stronger rDLPFC activity during memory suppression, reinforcing its role in reestablishing prefrontal control.
Sleep deprivation also disrupted the functional segregation of brain networks, with increased connectivity between the default mode network (DMN) and cognitive control network (CCN) and reduced DMN-thalamus connectivity, impairing adaptive control.
Finally, thought patterns were assessed using a multidimensional experience sampling method. Sleep-deprived participants reported fewer deliberate, task-focused thoughts, reflecting a broader breakdown in cognitive control.
Conclusions
To summarize, sleep deprivation significantly disrupts inhibitory memory control, impacting higher-order cognitive functions. Sleep-deprived participants showed impaired engagement of the rDLPFC during memory suppression, reducing their ability to downregulate unwanted memories over time.
In contrast, restful sleep, particularly a longer duration of REM sleep, was associated with enhanced rDLPFC activation, supporting prefrontal memory control.
Sleep deprivation also alters functional connectivity between brain networks, increasing DMN and CCN connectivity and reducing DMN-thalamus interactions. These disruptions coincided with fewer deliberate, on-task thoughts and highlighted sleep’s critical role in regulating memory and thought processes.
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