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Background: Although there was some evidence to suggest that the serotonergic system in the brain played an important role in premature ejaculation (PE), tryptophan hydroxylase‐2 (TPH2) is considered to be the key enzyme for the synthesis of 5‐hydroxytryptamine (5‐HT) and few studies have reported that brain TPH2 is involved in the regulation of ejaculation. Objectives: This study aimed to investigate whether changes in brain TPH2 levels were associated with PE and to explore the effects of acute administration of dapoxetine on TPH2 expression in the brain of rats with rapid ejaculation. Materials and methods: Based on the ejaculation frequency, the male rats were split into three groups: "rapid," "normal," and "sluggish" ejaculators. The level of 5‐HT in the brain was determined by an enzyme‐linked immunosorbent assay. TPH2 expression was detected by western blot analysis and immunohistochemistry. Results: The results showed that the concentration of 5‐HT and the expression of TPH2 in rapid rats were the lowest, while those in sluggish rats were the highest. Correlation analysis also indicated the level of TPH2 was positively correlated with ejaculation latency (r = 0.8633, p < 0.0001) and negatively correlated with ejaculation frequency (r = –0.874, p < 0.001). In addition, dapoxetine acute administration to rapid rats resulted in upregulation of TPH2 expression in the brain. Discussion: There was an important link between the level of TPH2 and the change of ejaculation behaviors. Decreased expression of TPH2 in relevant brain regions will lead to rapid ejaculation. Moreover, the effect of dapoxetine on prolonging ejaculation may be due to the upregulation of TPH2 expression. Conclusion: We found the correlation between the level of TPH2 in the brain and PE. The findings in this study will open up a novel way for future research in PE therapy. [ABSTRACT FROM AUTHOR]

Background Objective Methods Results Conclusion Sleep deprivation (SD) can cause damage to the male reproductive system. However, the duration required for such damage and the specific sequence and severity of damage to the testis and epididymis remain unclear.To investigate the effects of different durations of SD on different parts of the testis and epididymis caput, corpus, and cauda.Adult ICR mice were randomly assigned to five groups: the SD group (SD for 18 h/day for 1, 2, 3, or 4 weeks), the SD + Vit E group (supplemented with Vit E 50 mg/kg/d during 4 weeks of SD, the SD+NS group (saline supplementation during 4 weeks of SD), the SD + RS group (5 weeks of recovery sleep after 4 weeks of SD), and a normal sleep control (Ctrl) group. Following the interventions, sperm parameters, testicular and epididymal histopathology, inflammatory response, and oxidative stress markers were compared between the groups.Compared to the Ctrl group, the SD group showed a decrease in sperm motility and concentration from SD 2 W and SD 3 W, respectively. Decreases in sperm concentration and motility were more pronounced in the cauda compared to the caput and corpus. Pathological damage was less severe in the epididymis caput than in the corpus and cauda. After 4 weeks of SD, inflammation and oxidative stress increased in both testes and epididymis. Both sleep recovery and vitamin E supplementation showed significant improvements, though they did not fully reach the level of the Ctrl group.Chronic SD for more than 2 weeks causes varying degrees of damage to the testis, epididymis caput, corpus, and cauda in male mice. This damage is not fully reversible after 5 weeks of sleep recovery and antioxidant stress treatment. These findings help us to identify and prevent SD damage to the male reproduction at an early stage. [ABSTRACT FROM AUTHOR]