Spastic and non-spastic spinal cord injury induce systemic reproductive impairment via alterations in testicular morphology, microenvironment, spermatogenesis, and modulation of sperm parameters.

CONTEXT/OBJECTIVES: spinal cord injury (SCI) is frequently associated with male sexual dysfunction, including impaired spermatogenesis and poor semen quality. However, experimental models that accurately reflect injury-level-specific reproductive outcomes remain limited. This study aimed to establish thoracic (spastic) and sacral (non-spastic) SCI rat models and investigate differential effects on testicular architecture, microenvironment integrity, spermatogenesis, and sperm quality. DESIGN: Controlled in vivo experimental study. SETTING: Preclinical laboratory-based investigation. PARTICIPANTS: Adult male Sprague-Dawley rats: thoracic sham (T12 laminectomy), sacral sham (S2 laminectomy), thoracic SCI (T12 contusion), and sacral SCI (S2 contusion). INTERVENTIONS: Induction of level-specific spinal cord contusion injuries at thoracic (T12) and sacral (S2) segments, with sham-operated controls. OUTCOME MEASURES: Locomotor and sexual behavioral assessments (DPI 1-28); histological and molecular analysis of spinal cord and testicular tissues; evaluation of germ cell markers and blood-testis barrier (BTB) tight junction proteins; and quantitative sperm analysis (count, motility, viability, morphology). RESULTS: Thoracic and sacral SCI produced distinct behavioral phenotypes, confirming successful establishment of spastic and non-spastic injury models. Thoracic SCI resulted in marked locomotor impairment, whereas sacral SCI preserved locomotor function to a greater extent while producing pronounced sensory dysfunction and alterations in sexual behavior. Both injury models significantly impaired mounting, intromission, and ejaculation parameters. SCI was associated with degeneration of seminiferous tubules, reduced epithelial height, disruption of blood-testis barrier integrity, altered expression of tight junction proteins (Occludin and ZO-1), and suppression of spermatogenic markers including STRA8, SCP3, PIWIL1, and TNP1. These changes were accompanied by reductions in sperm viability, count, and motility, together with increased sperm morphological abnormalities. Collectively, the findings demonstrate that SCI induces systemic reproductive deficits extending from neural injury to testicular pathology and impaired sperm quality. CONCLUSION: SCI triggers a progressive pathophysiological cascade that extends beyond neural damag to impair male reproductive function. The established thoracic and sacral SCI models provide a robust, translational platform for studying injury-level-specific reproductive dysfunction and developing targeted therapeutic interventions.