Testicular histomorphometry and the proliferative and apoptotic activities of the seminiferous epithelium in Syrian hamster (Mesocricetus auratus) during regression owing to short photoperiod

Abstract

SUMMARYDuring the non-breeding season some animals exhibit testicular atrophy, decreased testicular weight and reduced seminiferous tubule diameter accompanied by depletion of the seminiferous epithelium. Some cellular factors involved in this depletion are changes in germ cell proliferation and apoptosis. In the Syrian hamster this depletion has been studied histologically and in terms of the involvement of proliferation and apoptosis in the seminiferous epithelium of fully regressed testes. The objectives of this study included the histomorphometrical characterization of the testis and the determination of the proliferative and apoptotic activity of germ cells in the seminiferous epithelium during testicular regression owing to short photoperiod. The study was performed using conventional light microscopy (hematoxylin and eosin), proliferating cell nuclear antigen and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP in situ nick end labelling staining, image analysis software, and transmission electron microscopy in three established regression groups: mild regression (MR), strong regression (SR), and total regression (TR). Morphometrically a gradual decrease in total tubular area and in the testicular, tubular, and epithelial volumes was observed during testicular regression. Interstitial and luminal volumes decreased from the MR group onwards. The tubular length decreased from MR to SR. As regards spermatogonial proliferation, only an initial decrease in proliferative activity was observed, whereas apoptotic germ cell activity increased throughout regression. The number of germ cells studied decreased throughout the process of testicular regression. In conclusion, testicular regression in Syrian hamster comprises two histomorphometrical phases, the first involving a decrease in seminiferous tubular diameter and volume and the second involving shortening of the seminiferous tubule and a decrease in interstitial volume. At the cellular level, there is an initial decrease in proliferation and increase in apoptosis involving all germ cells. At the end of regression, the proliferative and apoptotic activities of the spermatogonia recover the values observed prior to regression in preparation for recrudescence.

17β-estradiol effect on testicular β-endorphin expression in Psammomys obesus

“…We observed testicular b-endorphin expression in P. obesus in long photoperiod while in Syrian hamster Mesocricetus auratus [27], the level of POMC [28] and the b-endorphin immunoreactivity [28] were strong in short photoperiod. These data suggest that b-endorphin can play an important role in the regulation of seasonal gonadal activity depending on the species reproductive cycle.…”

Circannual Testis Changes in Seasonally Breeding Mammals

“…However, conclusive data in the Syrian hamster was only recently provided by Seco-Rovira et al [2014] showing that apoptotic incidence peaks during the period of testis regression and not later when the process has been completed, and the increase is high enough to explain a massive depletion of the germinative epithelium. The same authors also showed that apoptotic germ cells are phagocytized by Sertoli cells [Seco-Rovira et al, 2015]. An inverse rela- tionship between germ cell proliferation and apoptosis has been found during seasonal testicular changes in roe deer [Blottner et al, 1995[Blottner et al, , 1996Schön et al, 2004].…”

Testicular histomorphometry and the proliferative and apoptotic activities of the seminiferous epithelium in Syrian hamster during spontaneous recrudescence after exposure to short photoperiod

“…As a consequence of this reduction in gonadotropins, the testis atrophies or undergoes regression. In the case of the Syrian hamster ( Mesocricetus auratus ), testicular regression involves decreased testicular weight and volume and lower rates of androgen synthesis and spermatogenesis (Berndtson & Desjardins, ; Seco‐Rovira et al, ). This loss in spermatogenesis involves a depletion of the seminiferous epithelium with the arrest of spermatogenesis in primary spermatocytes (Hikim, Bartke, & Russell, ).…”

“…For other authors, the cause of reduced sperm formation in the nonbreeding season is the reduction in spermatogonia proliferation (Roelants, Schneider, Göritz, Streich, & Blottner, ). Recent studies in the Syrian hamster indicate that increased germ cell and Sertoli cell apoptosis, decreased spermatogonial proliferation and the phagocytosis of late spermatids would be the major causes of depletion of the seminiferous epithelium in the regression following a short photoperiod (Seco‐Rovira et al, , ).…”

“…In the Syrian hamster, low temperatures and hibernation may produce a delay in recrudescence due to increased apoptosis but without altering the proliferation of spermatogonia (Sato et al, ). At last, although the histomorphometry of regression has recently been described in the Syrian hamster (Seco‐Rovira et al, ), little is known about changes in the seminiferous epithelium in Syrian hamsters undergoing recrudescence as compared with the regressed state, other than the observed changes in testicular, interstitial and blood vessel volumes (Russell, Chandrashekar, Bartke, & Hikim, ).…”