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Impaired sperm function after spinal cord injury in the rat is associated with altered cyclic adenosine monophosphate
Shulun Wang1, Guichun Wang, Beverly E Barton
1Department of Surgery, Division of Urology, University of Medicine and Dentistry, New Jersey Medical School, Newark, NJ 07103, USA.
Abstract:
Our previous observations of changes in the expression of cAMP-dependent genes and the cAMP-responsive element modulator (CREM) in rat testicular cells after spinal cord injury (SCI) implied abnormal cAMP signaling as one of the mechanisms underlying the effects of SCI on spermatogenesis. It was postulated that such effects might contribute to abnormal sperm function after SCI. In this study, we examined this possibility. In spinal cord-contused (SCC) and -transected (SCX) rats, impaired sperm motility was accompanied by an increase in sperm cAMP content. Treatment of SCX rats with exogenous testosterone or follicle-stimulating hormone resulted in a further decrease in sperm motility, whereas sperm cAMP either increased or remained unchanged. These effects differed from those in sham control rats that received identical treatments. Results of these experiments also demonstrated that impaired sperm motility in SCC and SCX rats was accompanied by decreases in sperm viability and mitochondrial potential, thus suggesting a possible link between these changes. We concluded that impaired sperm motility after SCI was associated with decreases in sperm viability and mitochondrial potential. These effects occurred in the face of elevated sperm cAMP content and changes in its regulation, suggesting that altered cAMP signaling events might contribute to impairment of sperm motility and perhaps other sperm functions after SCI.
Insights
Spinal cord injury (SCI) impairs sperm motility, viability, and mitochondrial function in rats. This dysfunction is linked to elevated sperm cyclic adenosine monophosphate (cAMP) levels and altered cAMP signaling.
Area of Science:
- Reproductive biology
- Neuroscience
- Cellular signaling
Background:
- Spinal cord injury (SCI) affects spermatogenesis.
- Abnormal cAMP signaling is implicated in SCI-induced testicular changes.
- Previous studies noted altered cAMP-dependent gene expression and CREM in rat testicular cells post-SCI.
Purpose of the Study:
- To investigate the link between SCI, altered cAMP signaling, and impaired sperm function.
- To examine the effects of SCI on sperm motility, viability, and mitochondrial potential in rats.
Main Methods:
- Spinal cord contusion (SCC) and transection (SCX) models in rats.
- Assessment of sperm motility, viability, and mitochondrial potential.
- Measurement of sperm cyclic adenosine monophosphate (cAMP) content.
- Hormonal treatments (testosterone, FSH) in SCX rats.
Main Results:
- Impaired sperm motility in SCC and SCX rats correlated with increased sperm cAMP content.
- Hormonal treatments in SCX rats further decreased motility while affecting cAMP levels differently than in controls.
- Reduced sperm viability and mitochondrial potential were observed in SCC and SCX rats, linked to motility impairment.
- Elevated sperm cAMP content and altered regulation were noted in SCI rats.
Conclusions:
- Impaired sperm motility post-SCI is associated with decreased sperm viability and mitochondrial potential.
- Altered cAMP signaling, characterized by elevated sperm cAMP levels, may contribute to sperm dysfunction after SCI.
- These findings suggest a complex interplay between SCI, cAMP signaling, and male reproductive health.
