Differential expression of aromatase, estrogen receptor alpha and 17β-HSD associated with the processes of total testicular regression and recrudescence in the bat Myotis nigricans (Chiroptera: Vespertilionidae)

• M. nigricans express ERα in spermatogonia, elongated spermatids and Sertoli cells.
• M. nigricans express aromatase in spermatids and in Sertoli and Leydig cells.
• The total testicular regression process is regulated by testosterone and estrogen.
• Regulation occurs via production of T (17β-HSD), conversion into E2 (aromatase) and activation of AR and ERα.

Despite the worldwide distribution and many unique reproductive adaptations that bats present, many aspects of their reproductive hormonal regulation have not been adequately studied, especially in species that presented patterns of total testicular regression. Thus, this study aimed to evaluate the testicular expression of 17β-HSD type 1, aromatase and ERα in the bat Myotis nigricans, during the four periods of its reproductive cycle. Immunoreactivity for ERα was detected only in the cytoplasm of elongated spermatids and in the nuclei of spermatogonia and Sertoli cells. Expression of aromatase was observed in round and elongated spermatids and in Sertoli and Leydig cells. Immunoreactivity for 17β-HSD was restricted to the cytoplasm of Leydig cells. The three expression patterns varied significantly during the four periods of the reproductive cycle. Expression of ERα and aromatase in spermatids was continuous, while expression of ERα in spermatogonia occurred only in initial types (Ap). Expression of ERα and aromatase in Sertoli cells varied, with expression only in periods of spermatogenetic activities; and the same variation was observed for the expression of aromatase and 17β-HSD in Leydig cells. We, therefore, propose that the processes of total testicular regression and posterior recrudescence suffered by M. nigricans from September to January in the northwest of the São Paulo State of Brazil, are directly regulated by testosterone and estrogen. This occurs via the production of testosterone by 17β-HSD, its conversion into estrogen by aromatase, and activation/deactivation of Sertoli cells’ AR and spermatogonia’s ERα.