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PubMed1998

The establishment of spermatogenesis in the seminiferous epithelium of the pubertal golden hamster (Mesocricetus auratus).

The present study deals with initial spermatogenesis in the pubertal golden hamster (Mesocricetus auratus), in the course of which both the complex process of germ cell proliferation and differentiation and the cyclic pattern of organization of spermatogenesis are established. Germ cells pass through the complete sequence of spermatogenic differentiation from the A-spermatogonium up to the mature spermatid between days 12 and 38. During this period, germ cell development is already based on the pattern of organization and synchronization characteristic of adult spermatogenesis: 1. Judged by the germ cell types present, each of the successively appearing germ cell associations conforms to one of the adult stages of the seminiferous epithelium (stage conformity of the developmental steps of the pubertal seminiferous epithelium). 2. The overall intratesticular variance of the developmental levels reached in different tubular segments each covers almost exactly one cycle length of spermatogenesis. 3. There is a regular, continuous succession of developmental steps along the longitudinal course of the tubules which, in every single tubule, comprises the interval of one spermatogenic cycle ("wave" of the pubertal seminiferous epithelium). 4. Taken together, the latter two results indicate that the tubules of one given testis are equal to one another with respect to their developmental level, i.e., they develop synchronously. Germ cell propagation follows the clonal mode of proliferation. In quantitative terms, stage-related S-phase indices largely parallel the values of adult spermatogenesis. Both the frequently found germ cell apoptosis and degenerating intrameiotic spermatocytes correspond to degenerative phenomena in the adult seminiferous epithelium with respect to degenerative mode and stage-related occurrence. Germ cell development is closely related to the maturation of both Sertoli cells and Leydig cells. At two developmental phases, localized disturbances of germ cell differentiation occur which are specific to the pubertal period and which correlate with a maturational delay of Sertoli cells and Leydig cells, respectively: 1. Completion of Sertoli cell barrier formation may temporarily follow the initial onset of meiosis in the neighboring germ cells. As a result, mitotically dividing germ cells fall under the influence of a (hitherto hypothetic) "meiotic milieu" and characteristically degenerate (arrested germ cell mitoses). This relationship emphasizes the functional significance of the separation of the two seminiferous compartments and, in addition, heightens the understanding of the necessity of normal termination of Sertoli cell proliferation before germ cells initially enter meiosis. 2. The Leydig cell enzyme 11 beta-HSD, which is known to promote testosterone output, is established several days after the leading spermatids initially reach step 6 of spermiogenesis (which is immediately prior to the particularly testosterone-dependent start of elongation). The resulting selective developmental arrest of round spermatids of steps 6-6/7 between days 26 and 30 leads to a localized, partial desynchronization of the seminiferous epithelium, which can be traced for several days after the above-mentioned maturational delay of Leydig cells has been overcome and which is accompanied by an extensive degenerative disposition of the spermatids involved. The present investigation documents an organizational and synchronizational level of initial spermatogenesis that is similar to the situation in the adult animal. The analysis of temporarily occurring perturbations in the process of establishing the pubertal seminiferous epithelium emphasizes and specifies the close structural and functional relationships between the maturational state of somatic cells and germ cell differentiation.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1987

Spatial and temporal expression of cell surface galactosyltransferase during mouse spermatogenesis and epididymal maturation.

We have previously shown that sperm-egg recognition in the mouse is mediated by the binding of galactosyltransferase (GalTase) on the sperm surface to its appropriate glycoside substrate in the egg zona pellucida [L. C. Lopez, E. M. Bayna, D. Litoff, N. L. Shaper, J. H. Shaper, and B. D. Shur (1985) J. Cell Biol. 101, 1501-1510]. In the present study, we have defined the spatial and temporal expression of surface GalTase during spermatogenesis and epididymal maturation. Purified populations of spermatogenic cells were isolated by unit gravity sedimentation, and surface GalTase expression was determined by indirect immunofluorescence and by direct enzymatic assay. GalTase is present on the surface of all spermatogenic cells assayed. During differentiation, there is a progressive redistribution of GalTase from an initially diffuse and uniform localization on the surface of primary spermatocytes to a restricted plasma membrane domain overlying the dorsal aspect of the mature acrosome. This apparent redistribution of surface GalTase was confirmed by direct enzymatic assays, which show that surface GalTase activity, normalized per cell, remains relatively constant throughout spermatogenesis, despite a drastic reduction in cell surface area. When normalized to the relevant cell surface area, the GalTase concentration per square micrometer increases 77-fold from pachytene spermatocytes to cauda epididymal sperm. Cell surface GalTase is thought to be a cytoskeletally associated transmembrane protein [N. L. Shaper, P. L. Mann, and J. H. Shaper (1985) J. Cell Biochem. 28, 229-239]; consequently we examined whether cytoskeletal components may be involved in the redistribution of GalTase during spermatogenesis. beta-Tubulin, monomeric actin, and filamentous actin were found to be present during spermatogenesis, as assayed by indirect immunofluorescence and by Western immunoblotting. alpha-Actinin and vinculin were not detectable under these conditions and served as negative controls. During spermatogenesis, the distribution of tubulin coincides with the appearance of the mitotic spindle, flagellum, and manchette. On the other hand, the distribution of filamentous actin coincides with surface GalTase, suggesting that actin-containing microfilaments may participate in the redistribution of surface GalTase during spermatogenesis.

Animals↗
PubMed2002

Use of confocal microscopy for the study of spermatogenesis.

Spermatogenesis consists of spermatogonial proliferation, meiosis and spermatid differentiation. Laser scanning confocal microscopy (LSCM) may be used as an advanced analytical tool to follow spermatogenesis inside the seminiferous tubules without performing histological sections. For this purpose, separated seminiferous tubules are fixed in 0.5% paraformaldehyde, stained for DNA with propidium iodide and analyzed by LSCM. By producing longitudinal optical sections in the layer of spermatogonia, spermatocytes and spermatids, stage-specific changes in their structure may be followed within the tubules by LSCM. Longitudinal z-sections may be obtained to produce three-dimensional images of the seminiferous tubules. In addition, different proteins may be followed during spermatogenesis in a stage specific manner within the tubule by incubation of the fixed seminiferous tubules with appropriate antibodies. As an example of the spermatogenesis studies using described LSCM techniques, detailed examination of spermatogonia, spermatocytes and spermatids during golden hamster spermatogenesis is presented. LSCM analysis of c-kit and SC3 protein expression at different stages of hamster spermatogenesis is demonstrated.

Animals↗
PubMed2003

A stereological study of the effects of experimental inguinal cryptorchidism and subsequent orchiopexy on spermatogenesis in adult monkeys.

Our previous study demonstrated that experimental intra-abdominal cryptorchidism in adult rabbits for 13 weeks resulted in severe spermatogenic arrest: type A spermatogonia was the only germ cell type seen in the seminiferous epithelium and its number per testis was reduced by 84%. Seven weeks following orchiopexy, the type A spermatogonial number returned to the near-normal range in most animals and spermatogenesis partially recovered (Reproduction 2002, 124, 95-105). This study aimed to determine whether inguinal cryptorchidism would produce less-severe damage to spermatogenesis and whether subsequent orchiopexy would better restore spermatogenesis. Five normal adult male rhesus monkeys (Macaca mulatta) underwent bilateral artificial inguinal cryptorchidism. Half a year later, one testis together with the ipsilateral epididymis were removed from each animal and then unilateral orchiopexy was performed on the contralateral side, with the remaining testis and epididymis being removed another half a year later. A contemporary unbiased and efficient stereological tool, the optical disector, was used to estimate numbers of all types of spermatogenic cells in the testis and spermatozoa in the epididymis. Spermatogenic arrest was induced by cryptorchidism at the stage of spermatogonia (n = 1), spermatocytes (n = 2) or early spermatids (n = 1), with the type A spermatogonial numbers per testis being reduced to 14.8-57.2% of the control average; in one of the five cryptorchid animals, however, spermatogenesis remained normal. Subsequent orchiopexy, which was successfully performed on two animals with cryptorchidism-induced spermatogenic arrest, brought on a full or partial recovery of spermatogenesis. In conclusion, inguinal cryptorchidism induces less severe (in comparison with an intra-abdominal one) and variable damage to spermatogenesis, which is restored, at least in part, by subsequent orchiopexy.

Animals↗
PubMed1998

Genetic disorders and spermatogenesis.

Male infertility affects one man in twenty and a genetic basis seems likely in at least 30% of those men. Genetic regulation of fertility involves the inter-related processes of testicular development, spermatogenesis (involving germ cell mitosis, meiosis and spermatid maturation), and their endocrine and paracrine regulation. In regard to spermatogenesis, particular attention has been given to the Yq11 region, where some spermatogenesis genes ('azoospermia factors') appear to be located. Several candidate genes have been identified but have not been shown to have a defined or essential role in spermatogenesis. Microdeletions of Yq11 are found in approximately 15% of azoospermic or severely oligospermic men. The complexity of the genetic control of male fertility is demonstrated by the evidence for genes involved in spermatogenesis and sexual differentiation on the X chromosome and autosomes. Better understanding of the genetic regulation of normal spermatogenesis will provide new probes for clinical studies; however, at present the majority of spermatogenic failure remains without an identified genetic linkage. The advent of intracytoplasmic sperm injection permits fertility in many previously sterile men and presents the possibility of their transmission of infertility; appropriate counselling is required.

Aneuploidy↗
PubMed2004

Haploinsufficiency for the murine orthologue of Chlamydomonas PF20 disrupts spermatogenesis.

PF20 was first identified in Chlamydomonas rheinhardtii as an essential component of the axoneme central apparatus. We discovered that the mouse Pf20 gene encodes two major transcripts (2.5 and 1.4 kb), which are expressed in different patterns during spermatogenesis, yielding proteins of 71 and 35 kDa, respectively. Both proteins contain contiguous WD repeats in their C termini. The meiotically expressed 71-kDa protein is incorporated into the central apparatus, whereas the 35-kDa protein, which accumulates in postmeiotic male germ cells, is abundant in the nucleus. We disrupted the Pf20 gene domains that encode the C-terminal WD repeats in embryonic stem cells. Highly chimeric mice carrying the mutant Pf20 allele had impaired spermatogenesis with a significant loss of germ cells at the round spermatid stage, in association with disorganization of sperm axoneme structure. The mutated Pf20 allele was never transmitted, indicating that Pf20 haploinsufficiency caused the defects in spermatogenesis. The 35-kDa PF20 protein was shown to bind to meiosis-expressed gene 1 (MEIG1), a chromosome/chromatin-binding protein initially expressed during meiosis but retained in the germ cell nucleus throughout later stages of spermatogenesis. Our findings reveal an essential role for Pf20 in mouse spermatogenesis, sustaining postmeiotic germ cell viability. The different patterns of expression of the two PF20 proteins suggest the possibility that the Pf20 gene has multiple functions during spermatogenesis.

Animals↗
PubMed2006

Differential effects of spermatogenesis and fertility in mice lacking androgen receptor in individual testis cells.

Using a Cre-Lox conditional knockout strategy, we generated a germ cell-specific androgen receptor (AR) knockout mouse (G-AR(-/y)) with normal spermatogenesis. Sperm count and motility in epididymis from AR(-/y) mice are similar to that of WT (G-AR(+/y)) mice. Furthermore, fertility tests show there was no difference in fertility, and almost 100% of female pups sired by G-AR(-/y) males younger than 15 weeks carried the deleted AR allele, suggesting the efficient AR knockout occurred in germ cells during meiosis. Together, these data provide in vivo evidence showing male mice without AR in germ cells can still have normal spermatogenesis and fertility, suggesting the essential roles of AR during spermatogenesis might come from indirect cell-cell communication in a paracrine fashion. We then compared the consequences of AR loss in the spermatogenesis and fertility of G-AR(-/y) mice with two other testicular cell-specific AR(-/y) mice and total AR knockout male mice. The results provide clear in vivo evidence that androgen/AR signaling in Sertoli cells plays a direct important role in spermatogenesis and in Leydig cells plays an autocrine regulatory role to modulate Leydig cell steroidogenic function. Total AR knockout male mice have the most severe defects among these mice. These contrasting data with G-AR(-/y) mice suggest AR might have different roles in the various cells within testis to contribute to normal spermatogenesis and male fertility in mice.

Animals↗
PubMedDate not supplied

Control of spermatogenesis in primate and prospect of male contraception.

The present review is a summary of mechanisms of spermatogenesis in primates with emphasis on anti-spermatogenesis of testosterone (T), gossypol, and "testicular heat stress" for development of male contraception, Both FSH and testosterone stimulate all phases of spermatogenesis. FSH is capable of amplifying the population of the differential spermatogonia (B1, B2, B3 and B4) and controls the spermatogonia production rate, and, in synergy with testosterone, regulating spermatogenesis in adult monkeys. Pituitary FSH beta gene expression is governed by a feedback of Beta inhibin, which is a major component of the testicular negative feedback signals. Beta inhibin secreted by Sertoli cells is in turn inhibited by testosterone from Leydig cells under the control of LH. Disturbance of the normal interaction of pituitary FSH with Sertoli cell Beta inhibin is responsible for azoospermia or oligozoospermia induced by exogenous T. Three possible regimens of T, gossypol and "heat stress" have been suggested for male contraception. They act on different sites and stages of spermatogenesis in testis or sperm activity in epididymis. Apoptosis induced by testosterone occurs mainly at staged VII-VIII of spermatogenesis while that by testicular "heat stress" mostly occurs at stages I-IV and X-XII. Low dose of gossypol mainly influences the sperm activity in the epididymis although it also acts on testicular spermatids.

Animals↗
PubMed2001

Impaired spermatogenesis in men with congenital absence of the vas deferens.

It is generally assumed that men with congenital bilateral absence of the vas deferens (CBAVD) have azoospermia because of obstruction and that sperm production is normal. This study examines spermatogenesis in men with CBAVD to assess the validity of this assumption. We identified all men with CBAVD who had undergone either a diagnostic or therapeutic fertility procedure. Procedures included diagnostic biopsy, testis fine needle aspiration (FNA) mapping, microscopic epididymal sperm aspiration (MESA), and testis sperm extraction (TESE). Among 33 CBAVD men, 18 underwent testis biopsy, 27 had MESA/TESE, and 10 had FNA mapping. On evaluation of these procedures, normal spermatogenesis was present in 29 men. Four men (12%) demonstrated impaired spermatogenesis. One patient had FNA testis cytology consistent with late maturation arrest, another demonstrated hypospermatogenesis on biopsy and low sperm yield by MESA, and two patients had pure Sertoli cell only histology on biopsy. Aetiologies for impaired spermatogenesis included varicocele and underlying genetic abnormalities. Although patients with CBAVD are assumed to have normal spermatogenesis and infertility due simply to obstruction, the potential for concomitant defects in sperm production exists. A clinical suspicion of testis failure should prompt further diagnostic evaluation of spermatogenesis prior to sperm retrieval. In addition, genetic counselling should be offered and testing for genetic lesions, including cystic fibrosis gene mutations and/or variants, Y chromosome microdeletions, and karyotype abnormalities, should be considered.

Adult↗
PubMed2004

Idiopathic impaired spermatogenesis: genetic epidemiology is unlikely to provide a short-cut to better understanding.

The aetiology of impaired spermatogenesis is unknown in the majority of subfertile men. From several studies of concordance for involuntary childlessness among men, we can conclude that there is a substantial familial component in male subfertility and that shared loci segregating through families can be assumed. We now know that deletions on the Y chromosome, which do not penetrate fully, account for some of these cases. There are good reasons to suspect that other cases result from mutations in genes located elsewhere in the genome. In this article, we discuss different approaches to unravelling the molecular basis of impaired spermatogenesis originating from genetic abnormalities in chromosomes other than the Y chromosome. Genetic mapping studies are in general a good approach to detect disease-causing genes that are segregating through a population; they can provide a shortcut to unravelling the biochemistry of a disease. In this paper, we explain our reasons for arguing that linkage and association studies are no promising means to identify the genes causing impaired spermatogenesis. We conclude that direct screening of candidate genes for mutations will be necessary to detect genes involved in impaired spermatogenesis. However, this approach requires studies of the biochemical pathways of normal and abnormal spermatogenesis. Since we have a poor understanding of these pathways, more research is needed into the biochemistry of spermatogenesis.

Chromosomes, Human, Y↗
PubMed1993

Spermatogenesis is accelerated in the immature Djungarian and Chinese hamster and rat.

The rate of progression of spermatogenesis was studied in immature Djungarian and Chinese hamsters and Wistar rats by scoring the most advanced cell types present at various ages after birth. From 15 days of age onward, the most advanced cell types in the Djungarian hamsters were formed at a rate compatible with the duration of the spermatogenic cycle in adult animals, i.e., 7.9 days. However, in Djungarian hamsters up to 15 days of age, the rate of spermatogenic development was accelerated. The estimated duration of the spermatogenic cycle ranged between 5.0 and 5.3 days. In the rats, spermatogenesis also was accelerated during the first 15 days of life, with an estimated duration of the seminiferous cycle of 4.5-5.3 days. From 15 days of age onward, the rate of progression was strongly reduced, being compatible with the adult value of 12.8 days. In the Chinese hamsters, a similar change in the rate of spermatogenesis occurred at 25 days. Before this age, spermatogenesis proceeded with an estimated duration of the cycle of 8.8-9.2 days. From 25 days onward, spermatogenesis advanced much more slowly, at a rate compatible with the adult value of 17.0 days. Despite the strong reduction in the rate of spermatogenic progression in the three species, the cellular associations in the stages of spermatogenesis were not affected. In the three species, the clear reduction in the rate of spermatogenic progression correlated with the process of testicular descent, with the appearance of pachytene spermatocytes associated with preleptotene spermatocytes, and with the onset of tubular lumen formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2002

Apoptosis, onset and maintenance of spermatogenesis: evidence for the involvement of Kit in Kit-haplodeficient mice.

Kit/stem cell factor (SCF ) has been reported to be involved in survival and proliferation of male differentiating spermatogonial cells. This kinetics study was designed to assess the role of Kit/SCF during spermatogenesis in mice, and the extent of male programmed germ cell death was measured between 8 and 150 days of age. For this purpose, 129/Sv inbred mice in which one Kit allele was inactivated by an nlslacZ sequence insertion (Kit(W-lacZ/+)) were compared with 129/Sv inbred mice with wild-type alleles at the Kit locus. Four different approaches were used: 1) morphometric study to assess spermatogenesis, 2) flow cytometry to study testicular cell ploidy, 3) in situ end labeling to detect apoptosis, and 4) follow-up of reporter gene expression. Spermatogenesis was lower in Kit(W-lacZ/+) heterozygous mice both at the onset of spermatogenesis and during adulthood. Indeed, greater apoptosis occurred at the onset of spermatogenesis. This was followed in the adult by a smaller seminiferous tubule diameter and a lower ratio between type B spermatogonia and type A stem spermatogonia in Kit(W-lacZ/+) mice compared with Kit(+/+) mice. These differences are probably related to the Kit haplodeficiency, which was the only difference between the two genotypes. Germ cell counts and testicular cell ploidy revealed delayed meiosis in Kit(W-lacZ/+) mice. Reporter gene expression confirmed expression of the Kit gene at the spermatogonial stage and also revealed Kit expression during the late pachytene/diplotene transition. These results suggest involvement of Kit/SCF at different stages of spermatogenesis.

Alleles↗
PubMed1977

Relation of gonadotropin secretion by pituitary grafts to spermatogenesis in hypophysectomized rats.

In hypophysectomized male rats, 2 anterior pituitary (AP) grafts placed underneath the kidney capsule partially prevented atrophy of the testes and ventral prostate during a 17 day post-implantation period. Spermatogenesis was partially maintained as revealed by histological examination of the testes. The AP grafts released small amounts of LH and FSH and substantial amounts of prolactin as determined by radioimmunoassay. Serum LH and FSH were undetectable in the hypophysectomized rats with no AP grafts. Inhibition of prolactin release by daily injections of ergocornine methanesulfonate (ERG) did not significantly alter serum levels of FSH and LH, spermatogenesis or testes and ventral prostate weights, indicating that circulating levels of prolactin were not responsible for the partial maintenance of spermatogenesis and prostate weight in these rats. Daily injections of ovine prolactin also had no effect on spermatogenesis or prolactin also had no effect on spermatogenesis or prostate weight in the hypophysectomized rats, and there was no change in the histological appearance of the testes and prostate. These observations indicate that secretion of gonadotropins and not prolactin by AP grafts accounts for the partial maintenance of spermatogenesis and prostate weight in hypophysectomized, AP-grafted male rats during the experimental period studied.

Animals↗
PubMed2005

Levonorgestrel implants enhanced the suppression of spermatogenesis by testosterone implants: comparison between Chinese and non-Chinese men.

CONTEXT: Previous male contraceptive studies showed that progestins enhance spermatogenesis suppression by androgens in men. OBJECTIVE: We compared the efficacy of spermatogenesis suppression by the combination of levonorgestrel (LNG) with testosterone (T) implants to that by T implants alone in two different ethnic groups. DESIGN: This was a randomized trial performed in two centers with two treatment groups. SETTINGS: The study was performed at the Academic Medical Center in the United States and the Research Institute in China. PARTICIPANTS: Forty non-Chinese and 40 Chinese healthy male volunteers were studied. INTERVENTIONS: Subjects were randomized to receive four LNG implants together with four T implants (inserted on d 1 and wk 15-18) vs. T implants alone for 30 wk. MAIN OUTCOME MEASURES: The primary end point compared the efficiency of suppression to severe oligozoospermia (1 x 10(6)/ml) by LNG plus T implants vs. that by T implants alone. The secondary end point examined differences in spermatogenesis suppression between Chinese and non-Chinese subjects. RESULTS: LNG plus T implants caused more suppression of spermatogenesis to severe oligozoospermia during the treatment period than T implants alone at both sites (P < 0.02). In Chinese men, severe oligozoospermia was achieved in more than 90% of the men in both treatment groups. Suppression to severe oligozoospermia was less in the non-Chinese men (59%) after T alone (P < 0.020); this difference disappeared with combined treatment (89%). T implant extrusion occurred in six men. Acne and increased hemoglobin were the most common adverse events. CONCLUSION: T implants resulted in more pronounced spermatogenesis suppression in Chinese men. Addition of LNG implants to T implants enhanced the suppression of spermatogenesis in the treatment period in both Chinese and non-Chinese men.

Adult↗
PubMed2002

Identification of specific sites of hormonal regulation in spermatogenesis in rats, monkeys, and man.

A detailed understanding of the hormonal regulation of spermatogenesis is required for the informed assessment and management of male fertility and, conversely, for the development of safe and reversible male hormonal contraception. An approach to the study of these issues is outlined based on the use of well-defined in vivo models of gonadotropin/androgen deprivation and replacement, the quantitative assessment of germ cell number using stereological techniques, and the directed study of specific steps in spermatogenesis shown to be hormone dependent. Drawing together data from rat, monkey, and human models, we identify differences between species and formulate an overview of the hormonal regulation of spermatogenesis. There is good evidence for both separate and synergistic roles for both testosterone and follicle-stimulating hormone (FSH) in achieving quantitatively normal spermatogenesis. Based on relatively selective withdrawal and replacement studies, FSH has key roles in the progression of type A to B spermatogonia and, in synergy with testosterone, in regulating germ cell viability. Testosterone is an absolute requirement for spermatogenesis. In rats, it has been shown to promote the adhesion of round spermatids to Sertoli cells, without which they are sloughed from the epithelium and spermatid elongation fails. The release of mature elongated spermatids from the testis (spermiation) is also under FSH/testosterone control in rats. Data from monkeys and men treated with steroidal contraceptives indicate that impairment of spermiation is a key to achieving azoospermia. The contribution of 5alpha-reduced androgens in the testis to the regulation of spermatogenesis is also relevant, as 5alpha-reduced androgens are maintained during gonadotropin suppression and may act to maintain low levels of germ cell development. These concepts are also discussed in the context of male hormonal contraceptive development.

Androgens↗
PubMed1999

What are the germ cell phenotypes from infertile men telling us about spermatogenesis?

Drosophila mutants for known genes and those obtained following germline genetic engineering in mice have led to the identification of genes involved in the initiation and the maintenance of spermatogenesis and in the different steps of meiosis. Mutants allow the definition of meiosis-specific checkpoint controls that ensure the transmission of complete and undamaged genetic information. They reveal what spermatogenesis events are interdependent. In the light of these data, an attempt is made to define which events of spermatogenesis could be defective in some well-defined human spermatogenesis failures. They appear to be good models to study the decouplages of spermatogenesis events, the morphogenetic relationships between germ cell structures and the occurrence of pleiotropic sperm phenotypes. It is discussed whether a germ cell with a normal phenotype can transmit a non-functional gene involved in spermatogenesis and how homologous genes can lead to different germ cell phenotypes depending on the species.

Animals↗
PubMed1981

Testicular function of actively immunized male rats with LH releasing hormone (LHRH): a possible role of prolactin on regulation of spermatogenesis.

The effect of testosterone propionate (TP) on the recovery of spermatogenesis was compared in 3 types of experimentally induced gonadotropin-deficient rats; 1. hypophysectomized rats, 2. rats actively immunized to LHRH and 3. hypophysectomized and immunized rats bearing a pituitary isograft. In order to immunize animals to LHRH, deamidated LHRH conjugated with BSA (LHRH-BSA) was injected intradermally to male rats 4 times at 2 week intervals and additional booster injections continued once a month. Anti-LHRH titer was the highest on the 12th week and the titer remained at a relatively high levels thereafter. A remarkable decrease in testicular weight and testosterone production was achieved in 10 weeks associated with a drop in serum LH and FSH levels. In long term immunized rat (LIM rats) which had been immunized for more than 3 months, testicular atrophy advanced to a similar extent to that in long term hypophysectomized rats (HX rats). The administration of TP (1 mg/day) sc for 30 days restored spermatogenesis in LIM rats. The simultaneous administration of anti-LH and -FSH sera in addition to TP did not affect the restoration of spermatogenesis in LIM rats. The same TP treatment in HX rats, however, failed to restore spermatogenesis. Spermatogenesis was reinitiated after TP treatment if immunized-hypophysectomized rats received a pituitary isograft. Though the serum PRL level in LIM rats was one fifth of that in normal rats, a 2.5-fold rise in the PRL level was observed after TP treatment. These results suggest that PRL is involved in the process of spermatogenesis.

Animals↗
PubMed1987

Restoration of spermatogenesis by high levels of testosterone in hypophysectomized rats after long-term regression.

In order to correlate the levels of intratesticular testosterone and the status of spermatogenesis, the present study examined the spermatogenic responses of mature chronically hypophysectomized (HPX) rats to different regimens of testosterone (T) replacement, i.e. implantation of a 2 X 5 or 6 X 5 cm long testosterone capsule (TC), or injection of 25 mg or 100 mg of testosterone enanthate (TE) every 4 days for 90 days. These regimens restored the testicular testosterone of the HPX rats to 25-96% of that measured in normal control rats. The testis weight of untreated HPX rats was below 30% of the normal control values. It was restored to 60-80% of control values in the TC implanted rats and to 50% in those receiving TE injection. Complete spermatogenesis of HPX rats was restored in those receiving TC implants and 100 mg TE injections. It was incomplete in those given 25 mg TE injections. Quantitative evaluation of germ cells revealed that spermatogonial populations of HPX rats were restored to 70 and 50% of the normal levels in rats receiving TC implants and TE injection, respectively. Differentiation of these cells resulted in the population of preleptotene spermatocytes to the same extent as those observed in spermatogonia. The yield of spermatids in both TC- and TE-treated HPX rats was below 50% of normal controls. Ratios between two successive generations of germ cells in stage VII epithelium revealed both dosage and regimen effects upon the yield of meiotic cells and spermatids. These results suggest that both T concentration and the mode of T availability to the testis may be important for specific steps of germ cell development in different stages of the cycle of the seminiferous epithelium. The results of the present study demonstrate that as little as 25% of normal testicular T concentration is sufficient to support all stages of spermatogenesis. Failure to restore a normal germ cell number even in the presence of a normal testicular T concentration suggests the need of other factors for quantitative spermatogenesis. Furthermore, despite a higher testicular T concentration achieved by TE injections, the restoration of spermatogenesis was less pronounced by this regimen. This finding suggests that the consistency of testicular T may also be important for normal spermatogenesis.

Animals↗