The detrimental effects of spinal cord injury on spermatogenesis in the rat is partially reversed by testosterone, but enhanced by follicle-stimulating hormone

Our previous studies have demonstrated that impaired spermatogenesis during the acute phase of spinal cord injury (SCI) is preceded by a transient (bu t significant) suppression of serum FSH, LH, and testosterone (T) concentra tions. It is hypothesized that hormonal deprivation may impair Sertoli cell function, leading to the loss of spermatogonia, degeneration of spermatoge nic cells, and eventual regression of the seminiferous epithelium. The curr ent study examined the efficacy of exogenous T and FSH in the maintenance o f spermatogenesis and Sertoli cell functions in SCI rats. Implantation of T capsules (TC, 2 x 5 cm) attenuated some of the spermatoge nic lesions and maintained qualitatively complete spermatogenesis in all SC I rats 4 weeks after the surgery. In contrast, daily injections of 0.1 U of FSH alone, or in combination with TC implants, paradoxically enhanced the regression of spermatogenesis in SCI rats. At this time, the numbers of Aal , A1, and B spermatogonia and preleptotene spermatocytes in SCI rats have d ecreased by 25-30%. Though not prevented by TC implants, the decrease in Aa l and Al spermatogonia was attenuated by FSH alone but was further enhanced when FSH-treated rats also received TC implants. The intratesticular T con centration in untreated and FSH-treated SCI rats was not different from tha t of sham control rats, but it decreased by more than 95% in those SCI rats given TC implants alone. These results demonstrate that impairment of sper matogenesis during the acute phase of SCI is not related to the availabilit y of FSH and/or T. Northern blot analysis revealed an increase in androgen receptor messenger RNA (mRNA) in the testis of SCI rats; this increase was prevented by TC implants but persisted when FSH was also given. In contrast , the levels of FSH-receptor, androgen binding protein, and transferrin mRN A were not affected by SCI but were significantly higher in those SCI rats given FSH alone or in combination with TC. TC implants alone suppressed mRN A levels of transferrin in testes of SCI rat, without concomitant change in those for FSH-receptor and ABP. The changes in Sertoli cell responses to F SH and T, and perhaps other hormones, may alter signal events elicited by t hese hormones, thus contributing to abnormal epithelial environments and re gression of spermatogenesis. Maintenance of spermatogenesis in SCI rats by exogenous T suggests the feasibility of using exogenous hormones to impede the detrimental effects of SCI on spermatogenesis. This approach may have c linical applicability for the preservation of spermatogenic functions in SC I men.