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: lightpoet/Shutterstock.com
In a recent study published in Psychological and Cognitive Sciencesa team of researchers investigated how sleep deprivation impairs inhibitory control of memory and contributes to intrusive memories, focusing on the role of rapid eye movement (REM) sleep in restoring this function.
Background
Disturbing memories of unpleasant experiences can significantly affect mental health, especially in conditions such as depression, anxiety and post-traumatic stress disorder. Suppressing these memories helps to 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 memory retrieval in the hippocampus.
Sleep, particularly REM sleep, is crucial for the restoration of this mechanism, yet its exact role remains unclear. Further research is needed to clarify how disrupted sleep affects the neural and cognitive processes that underpin 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 wake times of up to 8:00 AM. and at least six hours of sleep a night. Written informed consent was obtained from all participants and they were compensated with £80 or academic credit.
Two participants were excluded because they did not comply with the study protocol, leaving a final sample of 85. Participants were randomly assigned to either a sleep deprivation group (n = 43) or a sleep rest group (n = 42).
Participants completed cognitive and affective tasks in two sessions — one in the evening and one the next morning. The sleep-deprived group remained awake under supervision, while the rested group had an eight-hour sleep opportunity monitored by polysomnography (PSG). Adherence to the protocol was confirmed using actigraphy wristwatches.
Tasks included memory encoding and suppression exercises, magnetic resonance imaging (MRI) scans, and emotional ratings. Functional magnetic resonance imaging (fMRI) assessed brain activity, while behavioral analyzes revealed reduced memory suppression in the sleep-deprived group, with higher intrusion rates compared to the sedated group.
These results highlight the critical role of sleep, particularly REM sleep, in effective memory control.
Study results
Sleep deprivation significantly reduces the brain’s ability to suppress disturbing memories. After 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 watched suppression attempts that failed and resulted in memory intrusions. Behavioral analyzes revealed that while suppression reduced intrusions over time for all participants, sleep-deprived subjects showed a slower decline, reflecting impaired adaptive memory suppression.
Interestingly, this impairment was not affected 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 the preliminary tasks before the nighttime interval, which may have influenced subsequent results.
However, by the final blocks of trials, the difference in intrusion rates between groups disappeared, suggesting that sleep deprivation primarily impedes improvement in sedation over time rather than overall sedation ability.
Heart rate variability (HRV), particularly the high-frequency component (HF-HRV), was examined to investigate physiological correlates of memory control. In the sleep-rested group, higher HF-HRV was associated with better sedation, whereas in sleep-deprived subjects, higher HF-HRV was unexpectedly associated with poorer sedation, suggesting that the benefits of HF-HRV depend on adequate 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.
At the same time, the right hippocampus, which is normally deactivated during sedation, showed reduced disengagement, indicating disrupted memory control circuits. Whole-brain analyzes confirmed these findings, with reduced prefrontal control and increased hippocampal activity following sleep deprivation.
REM sleep has been 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 restoring prefrontal control.
Sleep deprivation also disrupted the functional segregation of brain networks, with increased connectivity between the default mode network (DMN) and the cognitive control network (CCN) and decreased DMN-thalamus connectivity, reducing adaptive control.
Finally, thought patterns were assessed using a multidimensional experience sampling method. Sleep-deprived participants reported fewer purposeful, task-focused thoughts, reflecting a broader breakdown in cognitive control.
conclusions
In summary, sleep deprivation significantly disrupts the inhibitory control of memory, affecting higher-order cognitive functions. Sleep-deprived participants showed reduced rDLPFC engagement during memory suppression, reducing their ability to reduce unwanted memories over time.
In contrast, restful sleep, particularly longer REM sleep duration, 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 decreasing DMN-thalamic interactions. These disruptions coincided with less purposeful, on-task thinking and highlighted the critical role of sleep in regulating memory and thought processes.
