A study on mice found that a six-hour sleep disruption interfered with the consolidation of fear memories, making them weaker. This disruption also increased the levels of mRNA encoding brain-derived neurotrophic factor, a molecule implicated in changes to the brain region responsible for regulating fear responses. The paper was published in Neuropsychopharmacology.
Psychological trauma has a profound impact on sleep, often leading to persistent disturbances that affect overall well-being. Individuals who have experienced trauma frequently struggle with insomnia, as heightened stress and hyperarousal make it difficult to relax and fall asleep. Even when they do manage to sleep, many trauma survivors experience nightmares or night terrors, causing frequent awakenings and preventing deep, restorative rest.
This disrupted sleep pattern contributes to emotional instability, increasing the risk of anxiety and depression while exacerbating trauma symptoms. In particular, post-traumatic stress disorder (PTSD) is closely linked to chronic sleep problems, with many affected individuals reporting vivid nightmares that replay distressing events.
However, some studies suggest that sleep might also play a role in consolidating memories of traumatic events, potentially intensifying trauma symptoms. In contrast, if a person is prevented from sleeping for some time after a traumatic experience, they may have difficulty recalling certain details of the event. Studies on mice that underwent fear conditioning (i.e., learned to fear a previously harmless stimulus) showed that they had weaker recall of the learned fear when their sleep was disrupted within five hours after the event.
Study author Allison R. Foilb and her colleagues sought to examine the effects of a delayed, next-day sleep disruption on the expression of learned fear in mice. They also investigated how this disruption affected the expression of mRNA encoding brain-derived neurotrophic factor, a molecule involved in neuroplasticity—the brain’s ability to form new connections between neurons—in regions associated with the development, expression, and extinction of fear-related behaviors.
The study was conducted on adult male and female C57BL/6 mice, aged six to eight weeks. C57BL/6 mice are a widely used laboratory strain known for their black fur, strong immune response, and genetic stability. The mice had free access to food and water and were housed in individual Plexiglas cages in a temperature-controlled vivarium.
To condition the mice to fear a specific stimulus, the researchers paired a particular sound with an electric shock. Once the mice learned to associate the sound with fear, they were returned to their home cages and left undisturbed until the following morning.
Eighteen hours after the initial fear conditioning, the researchers divided the mice into two groups. One group was placed in a new cage, where they were periodically kept awake through mild environmental disturbances. These included introducing new objects into the cage to encourage exploration, touching the cage, or gently tapping the mice on their hindquarters. The goal was to prevent them from sleeping for the next six hours. The other group of mice was left undisturbed.
The results showed that mice exposed to sleep disruption exhibited a significant reduction in fear responses to the conditioned sound both immediately after the six-hour disruption and 24 hours later, compared to the undisturbed group. Additionally, this sleep disruption increased the levels of mRNA encoding brain-derived neurotrophic factor.
“These findings raise the possibility that the effects of our delayed sleep disruption regimen are not due to disruption of memory consolidation, but instead are caused by BDNF-mediated [brain-derived neurotrophic factor-mediated] neuroadaptations within the BLA [basolateral amygdala region of the brain] that actively suppress expression of fear. Treatments that safely reduce expression of fear memories would have considerable therapeutic potential in the treatment of conditions triggered by trauma,” the study authors concluded.
The study makes an important contribution to the scientific understanding of neural mechanisms underlying fear learning. However, it is important to note that the research was conducted on mice, not humans. While mice share many physiological similarities with humans, they are still distinct species, and results in humans may differ.
The paper, “Acute sleep disruption reduces fear memories in male and female mice,” was authored by Allison R. Foilb, Elisa M. Taylor-Yeremeeva, Brett D. Schmidt, Kerry J. Ressler, and William A. Carlezon Jr.
