The involvement of amyloid‐β in the central nervous system regulation underlying sleep deprivation‐induced rapid ejaculation in rats

Abstract

BackgroundAlthough some studies suggest that sleep deprivation may affect ejaculation regulation, related research is limited, and the mechanisms remain unclear.AimThis study aimed to explore whether sleep deprivation influences ejaculation regulation through amyloid‐beta and to investigate its potential mechanisms.Materials and methodsNormal ejaculating rats were randomly distributed into three separate groups for the study, and treated with sleep deprivation combined with saline gavage, sleep deprivation combined with sodium butyrate gavage, and control with saline gavage. The levels of amyloid‐beta and 5‐HT1A receptors were assessed through Western blotting, PCR, and immunohistochemical techniques. The levels of interleukin‐4 and serotonin (5‐hydroxytryptamine) in the brain were determined by enzyme‐linked immunosorbent assay.ResultsThe experiment showed that the rats in the sleep deprivation combined with saline gavage group rats had a significantly faster ejaculation compared to the control combined with saline gavage group rats. Meanwhile, sleep deprivation combined with saline gavage group had the highest levels of amyloid‐beta oligomers in the brain tissue. Correlation results revealed that the levels of amyloid‐beta oligomers in brain tissue were inversely related to ejaculation latency and positively associated with ejaculation frequency. Furthermore, we found that elevated levels of amyloid‐beta oligomers in brain tissue led to upregulation of 5‐HT1A receptor expression. Additionally, elevated levels of amyloid‐beta oligomers in brain tissue were found to increase interleukin‐4 levels, thereby reducing 5‐hydroxytryptamine levels.DiscussionSleep deprivation indeed accelerates ejaculation, and this acceleration is closely related to amyloid‐beta. Sleep deprivation can increase amyloid‐beta levels in brain tissue, mediating a decrease in 5‐hydroxytryptamine levels and overexpression of 5‐HT1A receptors, thereby accelerating ejaculation.ConclusionThere is a significant correlation between elevated amyloid‐beta levels in brain tissue because of sleep deprivation and accelerated ejaculation. This study's main findings offer insights into the development of acquired premature ejaculation linked to poor sleep and establish a theoretical framework for investigating potential treatments for this condition.