Effects of cellular prion protein on rapid eye movement sleep deprivation-induced spatial memory impairment
Li Hu1,2, Peng Li1, Zhendong You3
1Department of Neurology, Changzheng Hospital, Navy Medical University, Shanghai, 200003, P. R. China.
Abstract:
The effects of cellular prion protein on rapid eye movement sleep deprivation-induced spatial memory impairment were investigated, and the related mechanisms explored. Male C57BL/6 mice were randomly divided into four groups: environment control, sleep deprivation control, sleep-deprived-plasmid adeno-associated virus-green fluorescent protein group, and sleep-deprived-plasmid adeno-associated virus-cellular prion protein-green fluorescent protein group. Overexpression of cellular prion protein was induced by stereotaxic injection of adeno-associated viral plasmids-CAG-enhanced green fluorescent protein-cellular prion protein-Flag (a small label, which can be detected with corresponding tagged antibodies) into the hippocampus. Sleep-deprived mice were allowed no rapid eye movement sleep for 72 hours. Morris water maze was used to assess the effects of cellular prion protein on spatial learning and memory. The expression of amyloid-β was also investigated in all groups. The sleep-deprived- plasmid adeno-associated virus- cellular prion protein-green fluorescent protein group spent significantly more time in a goal quadrant compared with the sleep-deprived- plasmid adeno-associated virus-green fluorescent protein group. Sleep deprivation resulted in increased amyloid-β in the hippocampus, which was reversed by the overexpression of hippocampus cellular prion protein. Overexpression of cellular prion protein in the hippocampus rescues rapid eye movement sleep deprivation-induced spatial memory impairment in mice. It is shown that amyloid-β in the hippocampus might be one of the mechanisms.
Insights
Cellular prion protein overexpression in the hippocampus rescues spatial memory deficits caused by rapid eye movement sleep deprivation in mice. This suggests a role for amyloid-beta in the hippocampus.
Area of Science:
- Neuroscience
- Molecular Biology
- Sleep Science
Background:
- Rapid eye movement (REM) sleep deprivation is known to impair cognitive functions, including spatial memory.
- The role of cellular prion protein (PrPC) in sleep and memory is not fully understood.
- Amyloid-beta (Aβ) accumulation in the hippocampus is associated with memory impairment.
Purpose of the Study:
- To investigate the effect of cellular prion protein (PrPC) on spatial memory impairment induced by REM sleep deprivation.
- To explore the underlying mechanisms, particularly the involvement of amyloid-beta (Aβ).
Main Methods:
- Male C57BL/6 mice underwent 72 hours of REM sleep deprivation.
- Overexpression of PrPC in the hippocampus was achieved using adeno-associated virus (AAV) vectors.
- Spatial memory was assessed using the Morris water maze test.
- Hippocampal Aβ expression levels were measured.
Main Results:
- Mice overexpressing PrPC in the hippocampus showed improved performance in the Morris water maze compared to controls.
- REM sleep deprivation led to increased Aβ levels in the hippocampus.
- Overexpression of PrPC reversed the Aβ increase induced by REM sleep deprivation.
Conclusions:
- Cellular prion protein (PrPC) overexpression in the hippocampus can rescue spatial memory impairment caused by REM sleep deprivation.
- Amyloid-beta (Aβ) accumulation in the hippocampus may be a key mechanism underlying REM sleep deprivation-induced memory deficits.
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