Mediation of seasonal testicular regression by apoptosis

Abstract

Seasonal rhythms in physiology and behaviour are characteristic of most temperate and boreal species (Bronson, 1989). Synchronizing energetically demanding biological functions to the most favourable time of the year enables individuals to cope with recurring stressors such as seasonal declines in food or water availability, or annual fluctuations in ambient temperature. Environmental factors such as food availability, social cues, ambient temperature and the initial predictive cue of daylength (photoperiod) can facilitate or inhibit reproductive function seasonally. These factors maintain testicular function during favourable times of the year in some species (for example, birds), and induce testicular regression or atrophy when environmental conditions are less favourable in others (for example, small mammals). Environmental factors regulate testicular function through the hypothalamic-pituitary-gonadal (HPG) axis. Photoperiod serves as the primary predictive factor in the regulation of reproductive timing in long-and short-day breeding mammals and in most bird species (Wingfield and Kenagy, 1991;Bronson and Heideman, 1994). The general long-day breeding rodent response to seasonal changes in daylength is shown (Fig. 1); however, the actual HPG response to photoperiod is distinct among different species of birds, reptiles and mammals. Supplementary cues such as food and water availability also affect reproductive function directly, serving to fine-tune the initial, general reproductive response to photoperiod (Wingfield and Kenagy, 1991). Environmental factors that stimulate or maintain reproduction promote synthesis and secretion of GnRH from the hypothalamic median eminence, and positively regulate secretion of the gonadotrophins (LH and FSH) from the anterior pituitary (Bronson and Heideman, 1994). In contrast, non-stimulatory environmental factors decrease GnRH (pulse amplitude and frequency) release, resulting in testicular atrophy, reduced spermatogenesis and diminished testosterone production from Leydig cells, the steroidogenic somatic cells in the testicular interstitium (Sinha Hikim and Swerdloff, 1999).During the transition from the breeding to the nonbreeding state, males in most seasonally breeding species undergo 40-90% atrophy in testis mass. Cells must either undergo marked reduction in size, increases in the rate of cell death, or both, to achieve the reduction in volume observed during regression. The rate of cell division may decrease in the testis during regression, indirectly contributing to seasonal atrophy; however, total testicular DNA content in rodents is reduced with non-stimulatory photoperiod exposure, indicating an increase in cell death during regression (Desjardins and Lopez, 1983). Recent studies have examined complex changes that occur in testicular cells during seasonal reproductive regression. In this review, the contribution of apoptosis, or programmed cell death, in the mediation of seasonal atrophy is discussed. Specifically, the review focuses on the interactions of gona...

Apoptosis is not the cause of seasonal testicular involution in roe deer

“…Clear indications of a specific role for apoptosis in intensified elimination of testicular cells during seasonal testicular regression, as has been discussed for rodents (Young and Nelson 2001), have not been found in this study. The pronounced testis involution occurring after the rut in roe deer seems to be caused mainly by a rapidly diminishing proliferation of spermatogonia that starts long before the rut.…”

Follicle-Stimulating Hormone Regulates Both Sertoli Cell and Spermatogonial Populations in the Adult Photoinhibited Djungarian Hamster Testis1

“…Tissue distortion measurements for Bouins-fixed methacrylate-processed tissue have been made in our laboratory on a number of occasions [5,20], with negligible distortion observed, and thus, cell estimates were not adjusted. The mechanisms by which Sertoli cell populations retract and expand in this model remain unknown; however, mediation of seasonal testicular regression by apoptosis has been reported in the Djungarian hamster [37,38]. Cells undergoing apoptosis in this model have not been identified; however, apoptotic spermatogonia and spermatocytes have been reported in the photoinhibited Syrian hamster [39].…”

Testicular involution prior to sex change in gilthead seabream is characterized by a decrease in DMRT1 gene expression and by massive leukocyte infiltration

“…In seasonal breeding mammals, apoptosis occurs throughout the RC and is related with the amount of spermatogonia and spermatocytes present in the testis rather than being related with seasonal testicular involution [23,24]. However, in the gilthead seabream, apoptosis occurs during post-spawning in the first RC [16] and during post-spawning and testicular involution stages in the second, but not during spermatogenesis as occurs in others species [25,26].…”