Abstract
Objective: Rapid eye movement sleep deprivation (REM-SD) can cause a decline in learning and memory and lead to changes in behavior. Therefore, REM sleep plays a key role in processes that govern learning and memory. However, the mechanism underlying REM-SD-induced learning and memory impairment is unclear and the underlying molecular signaling still needs to be identified. In the present study, we investigated the role of the cPKCγ-Ng signaling pathway in REM-SD-induced learning and memory impairment.Method: Sixty male rats were divided into Control, REM-SD, REM-SD+cPKCγ activator PMA, REM-SD+cPKCγ inhibitor H-7, and sleep revival (SR) groups. The Morris water maze was used to assess spatial learning and memory. Western blot analysis was used to detect cPKCγ total protein expression and membrane translocation levels, and Ng total protein expression and phosphorylation levels.Results: The REM-SD group performed worse on the Morris water maze test than the control group. Western blot analysis showed that cPKCγ membrane translocation and Ng phosphorylation levels were significantly lower in the REM-SD group. SR following REM-SD restored learning and memory ability, cPKCγ transmembrane translocation, and Ng phosphorylation levels, but not to levels observed before REM-SD. PMA and H-7 significantly improved/disrupted task ability as well as cPKCγ transmembrane translocation and Ng phosphorylation levels in REM-SD rats.Conclusion: The REM-SD induced learning and memory impairment in rats and may be associated with the cPKCγ-Ng signaling pathway. Specifically, activation of the cPKCγ-Ng signaling pathway may protect against REM-SD.
Highlights
Sleep deprivation (SD) can cause changes in mood, learning, memory, and immune function, which can lead to physiological, psychological, and even behavioral changes
Levels did not differ between the Sleep Deprivation (SR) and control groups, between the rapid eye movement (REM)-SD and REM-SD+PMA groups, or between the REMSD and REM-SD+H-7 groups. cPKCγ protein expression in the SR group was significantly higher than that in the REM-SD group (Figure 5)
Western blot analysis showed that cPKCγ activity and Ng phosphorylation levels were significantly reduced following REM-SD, which suggests that REM-SD-induced impairments in spatial learning and memory in rats are associated with cPKCγNg signal transduction
Summary
Sleep deprivation (SD) can cause changes in mood, learning, memory, and immune function, which can lead to physiological, psychological, and even behavioral changes. Studies have confirmed that SD can cause obvious cognitive impairment [1,2,3], the underlying mechanisms remain unknown. Studies that focus on the molecular signaling pathways that govern this process will be important for the development of effective therapeutic interventions. REM-SD can cause a decline in memory and cognitive functions. Studies have found that some certain diseases, such as optic neuritis, sleep deprivation, etc., can cause changes in the topology of the brain network, which may cause symptoms of cognitive impairment [8]. Through the study of molecular signal targets, it may be possible to provide a new perspective for future drug interventions
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