Sleep deprivation, which is a common problem in modern society, impairs memory function and emotional behavior. TRPV1, a subfamily of transient receptor potential cation channels, is abundantly expressed in the central nervous system and is associated with animal behavior. In this article, we report that TRPV1 deficiency in mice alleviates sleep deprivation-induced abnormal behaviors. We found that in the sleep-deprived mice, TRPV1 knockout increased the duration and visits in the central area in the open field task and increased visits to the open arms in the elevated plus maze. The TRPV1-/- mice performed better during the test stage in the Morris water maze phase after sleep deprivation. In the mPFC and hippocampus regions, western blotting results showed that TRPV1-/- attenuated sleep deprivation-induced increases in GFAP, NLRP3, and ASC and increased the expression of the mitochondrial marker Tom20. Immunofluorescence results showed that the action of TRPV1 knockout on NLRP3 was negatively correlated with Tom20 after sleep deprivation. Our results confirm that TRPV1 knockout attenuates sleep deprivation-induced behavioral disorders. The effect of TRPV1 on the behavior of sleep-deprived mice may be related to the neuroinflammation associated with mitochondria in the mPFC and hippocampus.
Keywords: Emotion; Memory; NLRP3; Sleep deprivation; TRPV1.
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