Testicular regression and recrudescence in the bat Eptesicus furinalis: Morpho-physiological variations and hormonal signaling pathways

Males of the bat Eptesicus furinalis show at least one process of testicular regression, in which the testes regress and temporarily interrupt the production of sperm, during its annual reproductive cycle. As the process of spermatogenesis is under hormonal control, mainly of pituitary and androgen hormones, our aim was to analyze the morphological variations and the hormonal control of the testes of E. furinalis during the four phases of its reproductive cycle. Testes of 18 adult males, divided into four sample groups (active, regressing, regressed, and recrudescence phases), were submitted to morphological, morphometric, and immunohistochemical analyzes. The results demonstrate that the processes of testicular regression and recrudescence of E. furinalis are under the control of pituitary, androgen and estrogen hormones. The regulation is exerted mainly through the activation and cross signaling of AR and FSHR in Sertoli cells and of LHR in Leydig cells. The testicular regression appears to be activated by an inhibition/reduction of AR expression in Sertoli cells, which inhibits the proliferation and differentiation of new spermatogonia and causes the deactivation of spermatogenesis. Conversely, the testicular recrudescence occurs by the increasing of the expression of LHR in Leydig cells, and AR and FSHR in Sertoli cells, which reactivates the testicular production of androgens and estrogens, the proliferation of spermatogonia and restarts the spermatogenesis.

Automated summary

This study analyzed the morphological variations and hormonal control of the testes of Eptesicus furinalis bats during their reproductive cycle. The results showed that the regression and recrudescence of the testes are regulated by pituitary, androgen, and estrogen hormones through the activation and cross signaling of certain receptors in Sertoli and Leydig cells. Testicular regression is activated by a decrease in androgen receptor expression in Sertoli cells, while testicular recrudescence is initiated by an increase in luteinizing hormone receptor expression in Leydig cells, as well as androgen and follicle-stimulating hormone receptor expression in Sertoli cells.