In Macbeth, Shakespeare called sleep “the death of each day’s life,” but modern research suggests a very different role: sleep appears to protect and preserve memories.
New work from the Florida campus of The Scripps Research Institute (TSRI) combines neuroscience and psychological approaches to clarify how sleep supports memory. Published online ahead of print in the journal Cell, the study uses animal models to show that sleep suppresses the activity of specific dopamine-producing neurons that promote forgetting, thereby helping to preserve newly formed memories.
“Many scientists have concentrated on how memories form and stabilize,” said Ron Davis, chair of the TSRI Department of Neuroscience and senior author of the study. “Far less attention has been paid to forgetting, even though it is a fundamental brain function and could be crucial for developing memory-related treatments. Our study brings together the neuroscience of forgetting—how brain mechanisms produce forgetting—and psychological theories of how sleep influences retention into a single framework.”
Psychology and neuroscience have offered two complementary explanations for why sleep benefits memory. Behavioral studies emphasized that sleep reduces retroactive interference—new experiences or internal thoughts that can overwrite or disrupt a newly formed memory. Neuroscience has emphasized consolidation, the physiological strengthening and reorganization of memory traces during rest. The TSRI study links these perspectives by identifying a cellular mechanism that reduces forgetting during sleep.
The researchers focused on dopamine, a neurotransmitter well known for regulating brain plasticity—the capacity of neural circuits to change with experience. Prior work in Drosophila (fruit flies) showed ongoing activity in a subset of dopamine neurons drives forgetting of olfactory memories. The TSRI team examined how behavioral state—the distinction between active wakefulness and sleep—modulates this dopaminergic forgetting signal.
Using two independent approaches to increase sleep—the sleep-promoting drug Gaboxadol and genetic activation of sleep circuits—the investigators found that enhancing sleep reduced ongoing dopamine neuron activity and improved memory retention. By contrast, elevating arousal produced the opposite effect: increased dopaminergic signaling and faster forgetting. Crucially, the dopamine activity tracked the animal’s behavioral state, rising with movement and arousal and falling during periods of rest.
“Our data support a model in which sleep actively suppresses a neural forgetting signal, helping to preserve memories,” Davis explained. “As sleep deepens, dopamine neurons become less responsive to stimuli, which stabilizes memory traces.”
The findings do not negate sleep’s role in consolidation. Instead, the authors propose that reduced dopaminergic-driven forgetting and consolidation may act in parallel or sequentially. One intriguing possibility is that dampening the forgetting signal during sleep creates the necessary window for consolidation processes to operate more effectively, so both mechanisms together enhance memory retention.
Jacob A. Berry, research associate and first author, emphasized the translational relevance: “We know sleep benefits memory in humans and laboratory animals, and many genetic and circuit mechanisms are conserved. By showing that sleep quiets dopamine neuron activity that promotes forgetting, we provide a potential explanation for how sleep preserves memory across species.”
The paper, titled “Sleep Facilitates Memory by Blocking Dopamine Neuron-Mediated Forgetting,” lists Jacob A. Berry as first author and Ron Davis as senior author, with contributions from Isaac Cervantes-Sandoval and Molee Chakraborty of TSRI.
Funding: This research was supported by the National Institutes of Health (grants R37 NS19904 and R01 NS051251).
Source: Eric Sauter – Scripps Research Institute
Image credit: Public domain image used for illustration
Original research: Abstract for “Sleep Facilitates Memory by Blocking Dopamine Neuron-Mediated Forgetting” by Jacob A. Berry, Isaac Cervantes-Sandoval, Molee Chakraborty, and Ronald L. Davis in Cell. Published online June 11, 2015. doi:10.1016/j.cell.2015.05.027
Abstract
Sleep Facilitates Memory by Blocking Dopamine Neuron-Mediated Forgetting
Highlights
• Dopaminergic activity that underlies forgetting is regulated by behavioral state
• Sleep after learning improves memory by suppressing dopaminergic signaling
• Arousal accelerates forgetting by increasing dopaminergic signaling
Summary
Psychological studies have proposed that sleep supports memory by preventing retroactive interference from ongoing mental activity or external sensory input, while neuroscience work has focused on sleep-dependent consolidation processes that strengthen memories. In Drosophila, persistent activity in specific dopamine neurons has been shown to drive forgetting of olfactory memories. This study demonstrates that ongoing dopaminergic activity varies with behavioral state—rising during locomotion and arousal and decreasing during rest. Increasing sleep drive, whether pharmacologically with Gaboxadol or genetically by stimulating sleep circuits, reduces this dopaminergic activity and enhances memory retention. Conversely, elevating arousal boosts dopamine neuron signaling and speeds dopaminergic forgetting. These results indicate that forgetting is controlled by behavioral-state modulation of dopaminergic plasticity and help integrate psychological and neuroscientific perspectives on how sleep affects memory.