Biomedical subjects

L D Russell

Publications and source records attributed to L D Russell.

At least 37 records · Page 2Linked to original sources

PubMed1999

Globozoospermia in mice lacking the casein kinase II alpha' catalytic subunit.

Protein kinase casein kinase II (Ck2) is a cyclic-AMP and calcium-independent serine-threonine kinase that is composed of two catalytic subunits (alpha and alpha') and two regulatory beta-subunits. Ck2 is not a casein kinase in vivo, but over 100 substrates are known. The highly conserved amino acid sequences of its subunits and their broad expression suggest that Ck2 may have a fundamental role in cell function. Ck2 has been implicated in DNA replication, regulation of basal and inducible transcription, translation and control of metabolism. The Ck2alpha and Ck2alpha' isoforms (products of the genes Csnk2a1 and Csnk2a2, respectively) are highly homologous, but the reason for their redundancy and evolutionary conservation is unknown. We find here that Csnk2a2 is preferentially expressed in late stages of spermatogenesis, and male mice in which Csnk2a2 has been disrupted are infertile, with oligospermia and globozoospermia ('round-headed' spermatozoa). This is the first demonstration of a unique role for a Ck2 isoform in development. The primary spermatogenic defect in Csnk2a2-/- testis is a specific abnormality of anterior head shaping of elongating spermatids; this is the first defined gene that regulates sperm head morphogenesis. As the germ cells differentiate, they are capable of undergoing chromatin condensation, although many abnormal cells are deleted through apoptosis or Sertoli cell phagocytosis. The few that survive to populate the epididymis exhibit head abnormalities similar to those described in human globozoospermia, thus Csnk2a2 may be a candidate gene for these inherited syndromes.

Animals↗

PubMed1999

Development of germ cell transplants: morphometric and ultrastructural studies.

Mouse-to-mouse transplants were studied at 10 min, 9 h, 24 h, 1 week, 1 month, 2 months, and 3 months post-transplantation. Data from a previous light microscope study were confirmed and extended using morphometric and ultrastructural techniques. As soon as 10 min after introduction of the germ cells from one mouse into the tubule lumen of a recipient mouse they developed relationships with small Sertoli cell processes. The extent of this surface-to-surface relationship increased in animals sacrificed up to 1 week post-transplantation. Most transplanted germ cells retained the characteristics of the donor germ cells after they had been isolated and pelleted. Nearly all transplanted cells eventually underwent phagocytosis by the recipient Sertoli cells. The presence of small apparent clones of germ cells after 1 week of transplantation indicated that some germ cells may divide and survive for short periods within the epithelium. No discernible qualitative subcellular changes in the host Sertoli cell accompanying the development of transplant spermatogenesis were noted. Macrophages were present in the region of the boundary tissue between myoid cells and appeared to increase in number in the peritubular tissue of transplanted testes. Images suggest that they migrated into the tubule to gain entrance to the lumen and there take on the form of activated macrophages. Some macrophages phagocytose sperm at 2 months and 3 months post-transplantation. A testis weight increase previously demonstrate to occur at 24 h post-introduction of germ cells was found to be due to an increase in the volume of the tubular lumen. The increase of lumen size at 24 h was not related to the volume of the injected material. It is suggested that the presence of injected cells, likely germ cells, in the tubule lumen stimulated increased secretion by the Sertoli cell.

Animals↗

PubMed1998

Testicular degeneration in Bclw-deficient mice.

To identify genes required for mammalian spermatogenesis, we screened lines of mutant mice created using a retroviral gene-trap system for male infertility. Homozygous ROSA41 male mice exhibit sterility associated with progressive testicular degeneration. Germ-cell defects are first observed at 19 days post-natal (p19). Spermatogenesis is blocked during late spermiogenesis in young adults. Gradual depletion of all stages of germ cells results in a Sertoli-cell-only phenotype by approximately six months of age. Subsequently, almost all Sertoli cells are lost from the seminiferous tubules and the Leydig cell population is reduced. Molecular analysis indicates that the gene mutated is Bclw, a death-protecting member of the Bcl2 family. The mutant allele of Bclw in ROSA41 does not produce a Bclw polypeptide. Expression of Bclw in the testis appears to be restricted to elongating spermatids and Sertoli cells. Potential roles for Bclw in testicular function are discussed.

Age Factors↗

PubMed1998

Development of germ cell transplants in mice.

Development of spermatogonial transplants was studied by using 5- to 6-wk-old histocompatible mice as cell donors and sterile (W-locus) mice as recipients. Groups of animals transplanted with germ cell suspensions were killed at 10 min, 9 h, 24 h, 1 wk, 1 mo, 2 mo, and 3 mo along with age-matched "start" and "end" W-locus controls. Weight of testes increased significantly at 24 h through 3 mo after germ cell transplantation, suggesting that the infused cells quickly stimulated organ function. Small clones of young spermatocytes were evident at 1 mo and sperm at 2 mo. The percentage of tubular profiles containing active spermatogenesis originating from spermatogonia increased with time (0.8% at 1 mo, 8.9% at 2 mo, and 28.2% at 3 mo). Most transplanted germ cells were eliminated from the seminiferous epithelium through phagocytosis by Sertoli cells that occurred primarily before 1 wk, although some pachytene cells were able to proceed through meiosis by 1 wk. A variety of abnormal features are described that characterize developing spermatogenesis in the transplanted testis. Spermatogenesis improved quantitatively and qualitatively with time although released sperm were frequently engulfed by intratubular macrophages and Sertoli cells. A quantitative analysis of spermatogenesis from transplanted germ cells will serve as a basis for improving spermatogonial transplant efficiency.

Animals↗

PubMed1998

Germ cell genotype controls cell cycle during spermatogenesis in the rat.

Spermatogenesis is one of the most productive self-renewing systems in the body: on the order of 10(7) spermatozoa are produced daily per gram of testis tissue. In each mammalian species, the time required for completion of the process is unique and unalterable. Because the process is supported by somatic Sertoli cells, it has generally been thought that cell-cell interaction between germ and Sertoli cells controls the duration of cell cycles and cellular organization. We have used the newly developed technique of spermatogonial transplantation to examine which cell type(s) determines the rate at which germ cells proceed through spermatogenesis. Rat germ cells were transplanted into a mouse testis, and the mouse was killed 12.9-13 days after administration of a single dose of [3H]thymidine. The most advanced rat cell type labeled was the pachytene spermatocyte at stages VI-VIII of the spermatogenic cycle. In animals given only rat cells, some endogenous spermatogenesis of the mouse recovered. The most advanced labeled mouse cell types in recipients killed 12.9-13 days after administration of a single dose of [3H]thymidine were meiotic cells or young spermatids, which is consistent with a spermatogenic cycle length comparable to the 8.6 days reported for the mouse. The same results were obtained if a mixture of rat and mouse cells were transplanted. There existed two separate timing regimens for germ cell development in the recipient mouse testis; one of rat and one of mouse duration. Rat germ cells that were supported by mouse Sertoli cells always differentiated with cell cycle timing characteristic of the rat and generated the spermatogenic structural pattern of the rat, demonstrating that the cell differentiation process of spermatogenesis is regulated by germ cells alone.

Animals↗

PubMed1997

Radiation-induced cell death in the mouse testis: relationship to apoptosis.

The killing of male germ cells by radiation and other toxicants has recently been attributed to apoptosis, but a critical evaluation of the presence of the different features of apoptosis has not been performed. In this study, mouse testes exposed to radiation were examined by light microscopy, electron microscopy and terminal transferase-mediated end labeling (TUNEL) to determine whether the cells were apoptotic according to several criteria. Testes were irradiated with single doses of gamma rays of up to 5 Gy. Although the maximum response was produced by 5 Gy, even 0.5 Gy induced marked changes. The numbers of abnormal spermatogonia reached a peak 12 h after irradiation and then declined, and the total number of spermatogonia began to decline at 12 h. These changes were most prominent among the B spermatogonia and early preleptotene spermatocytes. When examined by both light and electron microscopy, the majority of the abnormal spermatogonia showed condensation of nuclear chromatin and some showed features similar to necrosis, but the typical morphological characteristics of apoptosis, margination of chromatin and nuclear fragmentation, were rare. Many of the abnormal spermatogonia were TUNEL-positive, with the maximum number occurring at 12 h after irradiation. Although the morphological features of radiation-induced spermatogonial degeneration were not typical of apoptosis, the TUNEL staining, the rapid onset of degeneration and the sensitivity to low doses suggest that the mechanism of radiation-induced spermatogonial degeneration is closely related to apoptosis.

Animals↗

PubMed1996

Testis of prepubertal rhesus monkeys receives a dual catecholaminergic input provided by the extrinsic innervation and an intragonadal source of catecholamines.

The mammalian testis is innervated by extrinsic catecholaminergic nerves and responds to catecholamines with steroid secretion. Although the primate testis has also been shown to be innervated, potential differences in the density of this innervation between immature and sexually developed individuals have not been described. A recent study demonstrated that the primate ovary contains a network of neuron-like cells and that some of these cells are catecholaminergic. It is thus possible that the male gonad is also endowed with a similar intragonadal source of catecholamines. The present study addresses these two issues. Catecholaminergic nerves were identified as such by their content of immunoreactive tyrosine hydroxylase (TH; the rate-limiting step in catecholamine biosynthesis), and in some cases by glyoxylic acid histochemistry. Fibers containing TH were abundant in testes from juvenile animals (1-2 yr of postnatal life), but the density of this innervation was not maintained in adult animals, whose testis showed only a few TH-positive fibers scattered in the interstitial tissue. Testicular norepinephrine (NE) concentration was much lower in adult than in juvenile animals, suggesting that the marked increase in testicular weight that occurs with the attainment of sexual maturity is not accompanied by corresponding changes in NE content. At the ultrastructural level, testicular nerve fibers contained pleiomorphic, dense-core and clear vesicles, suggesting the presence of catecholamines and other neurotransmitters. In addition to this extrinsic catecholaminergic innervation, prepubertal testes, but not adult gonads, contained an intrinsic population of TH-immunopositive neuron-like elements, identified as cells by confocal scanning laser microscopy. To determine whether the prepubertal monkey testis indeed expresses the TH gene, testicular RNA was subjected to reverse transcriptase polymerase chain reaction to amplify the 5' end of TH mRNA, which encodes the regulatory domain of the enzyme. The cDNA that was obtained predicts an amino acid sequence similar, but not identical, to that encoded by the alternatively spliced type 1 TH mRNA form present in the adrenal gland. These results indicate 1) that the primate testis receives a dual catecholaminergic input, one provided by the extrinsic innervation and the other by neuron-like cells located within the gonad itself, and 2) that the influence exerted by both sources on testicular function may be more prominent during the prepubertal period than in adulthood. The presence in the testis of a TH mRNA variant encoding amino acid substitutions in its 5' end suggests that regulation of testicular TH enzyme activity may include a gonad-specific component.

Aging↗

PubMed1995

Morphometry of rat germ cells during spermatogenesis.

BACKGROUND: There has never been a study of the components of germ cells as they progress through spermatogenesis. METHODS: The structural changes taking place in rat germ cells, from spermatogonia to late spermatids, were studied utilizing morphometric techniques conducted largely at the ultrastructural level. RESULTS: Volume and surface area parameters for virtually all cellular and subcellular features were obtained for nine periods during the spermatogenic cycle. Virtually all germ cell components show dynamic properties associated with specific phases of their development. CONCLUSIONS: The data provided can be used in an objective way to characterize structural changes taking place during spermatogenesis and to relate those structural changes to functional properties of germ cells.

Acrosome↗

PubMed1995

Neonatal hypothyroidism causes delayed Sertoli cell maturation in rats treated with propylthiouracil: evidence that the Sertoli cell controls testis growth.

BACKGROUND: The testes of rats treated neonatally with propylthiouracil (PTU) grow to almost twice their normal size. The cause of testicular enlargement has been suggested to be the result of delayed maturation of Sertoli cells, allowing Sertoli cell division to occur beyond the 15th postnatal day, the commonly recognized cutoff date for Sertoli cell divisions. It has been shown that an increased population of Sertoli cells in postnatal development supports increased numbers of germ cells in adult animals. After examining developing rats treated neonatally with PTU, we hypothesized that an approximate 10-day delay in maturation was occurring and proceeded to test this hypothesis experimentally. Thus the purpose of this report was to determine if a 10-day delay in maturation could explain the increased numbers of Sertoli cells and increased testis size in PTU-treated animals. METHODS: Both control animals and animals treated neonatally with PTU N = 5/group were sacrificed at 15 and 25 days of age and prepared for electron microscopy. RESULTS: Micrographs show and morphometric ultrastructural analysis of numerous parameters demonstrated at the 95% probability level that Sertoli cells from 25-day-old PTU animals are not different in size and most constituents (volume and surface area) from 15-day-old control animals and are less mature than 25-day-old control animals. Mitosis of Sertoli cells was observed in PTU-treated animals in 25-day-old animals but not in age-matched controls. The number of Sertoli cells in 25-day-old PTU-treated animals is significantly increased over age-matched controls. Micrographs show the presence of immature Sertoli cell nuclei in 25-day-old animals receiving PTU as well as increased germ cell degeneration in this group. Sertoli cell tight junction formation is also delayed in PTU-treated animals as compared with controls. CONCLUSIONS: Together, the data show that delayed maturation of Sertoli cells occurs in treated animals that corresponds to a minimum of 10 developmental days. In the immature state, Sertoli cells continue to divide. Data presented herein and published data related to PTU treatment indicate that delayed maturation of the Sertoli cell results in delayed maturation and proliferation of other testicular cell types. From this and from published data, the hypothesis is presented that the Sertoli cell is responsible for the overall control of testis development.

Animals↗

PubMed1995

Increased accessibility of the N-terminus of testis-specific histone TH2B to antibodies in elongating spermatids.

Changes in chromatin structure during spermatogenesis were investigated using a monoclonal antibody that immunoreacts with the N-terminus of the testis-specific histone TH2B. This monoclonal antibody, which had been raised against rat tyrosine hydroxylase (TH), cross-reacted with TH2B because of sequence homology at the N-termini of TH and TH2B. The epitope was localized to the N-terminus of TH2B as trypsin-digested chromatin which lacked the N-terminal tail did not react with anti-TH and preincubating anti-TH with a synthetic peptide made from the homologous sequence between TH2B and TH inhibited its binding to TH and TH2B. In histological sections of rat testis, the primary spermatocytes and round spermatids immunoreacted weakly, whereas elongating spermatids at steps 10-12 immunoreacted intensely with anti-TH. Increased staining of elongating spermatids was also observed in mouse and hamster by immunohistochemistry. However, immunoblotting proteins extracted from separated rat testis cells showed no increase in the TH2B content of these late steps of spermatids. The apparent increase in the immunohistochemical staining corresponds to increased accessibility of the epitope in the elongating spermatids. This indicated that the N-terminus of TH2B is less tightly bound to DNA or to other proteins at this time in preparation for the removal of TH2B and other histones.

Amino Acid Sequence↗

PubMed1995

Characteristics of mitotic cells in developing and adult testes with observations on cell lineages.

This report describes characteristics of dividing cells, primarily in developing (10-40 day) rat testis and relates the structure of the dividing cells to the structure of interphase cells. Mitotic cells were characterized in seven zones. Dividing Sertoli cells were seen prior to day 15 and possessed distinct characteristics as compared with dividing germ cells. Myoid cells showed morphological characteristics of precursor myoid cells; 'clear cells' self-replicated in the myoid cell layer; adult-type Leydig cells, some containing lipid, differentiated early (10th-15th postnatal days) from fibroblast-like cells of the multilayered tubule wall and later (15th-25th postnatal days) from dividing differentiated and semi-differentiated Leydig cells within the lymphatic space; fibroblastic cells arose from cells with similar morphological characteristics; semi-differentiated Leydig cells divided, and differentiated Leydig cells in the lymphatic space self-renewed; undifferentiated perivascular cells most likely gave rise to Leydig cells, pericytes; arteriolar smooth muscle cells and vascular endothelial cells arose from division of the pre-existing respective cell types. Fetal Leydig cells appeared to remain but, with time, they appeared to lose their lipid. The data suggest that (1) early recruitment of Leydig cells from undifferentiated peritubular fibroblast-like cells, (2) later mitosis of differentiated and semi-differentiated Leydig cells primarily in the interstitium but also in the perivascular region, and (3) the continued presence of pre-existing Leydig cells from the fetus constitute the adult population. Leydig cell division in the adult mouse was documented. This study provides the necessary information for the recognition of cell divisions to study of cell lineages among testis cells.

Animals↗

PubMed1995

Building a testis.

Specific cellular, subcellular and acellular components of the rat testis including the capsule, the peritubular tissue (tunica propria) and the lymphatic endothelium were analyzed using morphometric techniques at cellular and subcellular levels to yield volume and surface area data. These data were integrated with previously published data for other cellular components of the rat testis to provide information about the volumetric composition for virtually every component of this organ. For major cell types (Leydig, Sertoli, myoid cells and germ cells) the data are expressed to the subcellular level in terms of volume and, in some instances, surface area. Graphic portrayals of testis constituents are used for rapid visual understanding of testis structure. The data presented herein are useful in conjunction with biochemical data to describe physiological properties of cells and cell components and also for understanding how structure differs under experimental and in pathological situations.

Animals↗

PubMed1995

Infertility in a transgenic rat due to impairment of cytoplasmic elimination and sperm release from the Sertoli cells.

In line TGR(mRen2)26 transgenic rats (TGR26) bearing a randomly inserted additional renin transgene, the males, but not the females, were found to be infertile. Tissue was obtained from TGR26 males and littermate controls after perfusion fixation, and the morphology of the testes and epididymides was examined. Testis size was normal as was gross morphology, but careful examination revealed that the release of many spermatozoa at stage IX of the spermatogenic cycle was impaired. In addition, the process of cytoplasmic elimination was abnormal, as cytoplasmic fragments of elongate spermatids were present in the epididymis. In TGR26 males, seminiferous tubule lumen size was significantly larger (p < 0.001) than in littermate controls, a difference that was most marked at stages IX-XIV--an effect that could be related to the retention of spermatozoa. In situ hybridization confirmed that expression of renin mRNA could be detected in testes of TGR26 rats but not in normal controls or in a fertile line (TGR27) of rats bearing the same transgene. Immunocytochemistry and in situ and Northern hybridization were used to elucidate the pattern of expression of genes that previous studies have implicated in the process of sperm maturation and/or release. Of the gene products examined (sulphated glycoproteins 1 and 2 [SGP-1, SGP-2], transition proteins 1 and 2 [TP-1, TP-2], urokinase, and cyclic protein 2[CP-2], none showed any major change in the pattern of expression compared with that in controls. We postulate that TGR26 transgenic male rats may be infertile because the expression of a gene (or genes) involved in the process of cytoplasmic elimination and/or sperm release has been disrupted by the presence of the transgene close to or within the gene(s). Future planned studies will involve determination of the insertion site(s) and ultrastructural analysis of the final phases of spermiogenesis.

Animals↗

PubMed1995

Infertility in a transgenic rat due to impairment of cytoplasmic elimination and sperm release from the Sertoli cells.

In line TGR(mRen2)26 transgenic rats (TGR26) bearing a randomly inserted additional renin transgene, the males, but not the females, were found to be infertile. Tissue was obtained from TGR26 males and littermate controls after perfusion fixation, and the morphology of the testes and epididymides was examined. Testis size was normal as was gross morphology, but careful examination revealed that the release of many spermatozoa at stage IX of the spermatogenic cycle was impaired. In addition, the process of cytoplasmic elimination was abnormal, as cytoplasmic fragments of elongate spermatids were present in the epididymis. In TGR26 males, seminiferous tubule lumen size was significantly larger (p < 0.001) than in littermate controls, a difference that was most marked at stages IX-XIV--an effect that could be related to the retention of spermatozoa. In situ hybridization confirmed that expression of renin mRNA could be detected in testes of TGR26 rats but not in normal controls or in a fertile line (TGR27) of rats bearing the same transgene. Immunocytochemistry and in situ and Northern hybridization were used to elucidate the pattern of expression of genes that previous studies have implicated in the process of sperm maturation and/or release. Of the gene products examined (sulphated glycoproteins 1 and 2 [SGP-1, SGP-2], transition proteins 1 and 2 [TP-1, TP-2], urokinase, and cyclic protein 2 [CP-2]), none showed any major change in the pattern of expression compared with that in controls. We postulate that TGR26 transgenic male rats may be infertile because the expression of a gene (or genes) involved in the process of cytoplasmic elimination and/or sperm release has been disrupted by the presence of the transgene close to or within the gene(s). Future planned studies will involve determination of the insertion site(s) and ultrastructural analysis of the final phases of spermiogenesis.

Animals↗

PubMed1994

Insertional mutation that causes acrosomal hypo-development: its relationship to sperm head shaping.

A family of transgenic mice (OVE 219) was generated by microinjection of a tyrosinase minigene (Ty811C). The transgenic mice demonstrate an atypical and variable coat color pattern and the homozygous males show abnormalities of spermatogenesis that are variably expressed from animal to animal. Heterozygous mice proved to have normal spermatogenesis and along with non-transgenic mice were used as controls to study the abnormalities in spermatogenesis in OVE 219 homozygous males. These abnormalities shed light on the features controlling normal spermatogenesis. In some homozygous males early spermiogenesis was disrupted as the flagellar microtubules became disorganized within the flagellar process. What appeared to be crystalline tubulin was noted within some of the rounded flagellar processes. Sperm with this defect did not develop a flagellum. In other homozygous males defects were apparent by step 6 or 7 of spermiogenesis when the acrosome did not grow and spread over the nucleus as noted in control animals. The modified nuclear envelope underlying the acrosome continued to develop and spread well beyond one margin of the acrosome. Since the modified nuclear envelope grew independently of the acrosome, the acrosome was not the controlling factor in determining the spread of the modified nuclear envelope. Micrographs revealed that Sertoli ectoplasmic specialization failed to form over most regions of the spermatid head lacking a normal acrosome. In homozygous males, the manchette took origin (proximally) in close relation to the modified nuclear envelope and never in relation to the edge of the spreading acrosome, a feature indicating that manchette placement was influenced by the position of the modified nuclear envelope and not the edge of the acrosome. Thus the modification in the nuclear envelope may be the primary event to signal acrosomal spread and manchette development. In spermatids where the manchette developed from an ectopic site, the result was abnormal caudal head shaping. In some spermatids a portion of the manchette was lacking. When this occurred the caudal head was rounded in the region of the missing manchette. In a minority of spermatids there was no evidence for a manchette. The entire caudal head was gently rounded. These data support the growing body of evidence that the caudal sperm head is shaped, in part, by the manchette. The OVE 219 family of mice provides a useful model to understand the processes involved in periods of spermiogenesis that are critical to development of a normally shaped sperm head.

Acrosome↗

PubMed1994

Sertoli cells in testes containing or lacking germ cells: a comparative study of paracrine effects using the W (c-kit) gene mutant mouse model.

BACKGROUND: Paracrine effects of germ cells on Sertoli cell structure were examined in a mouse model with the W locus (dominant white spotting) mutation in which animals with the W/Wv genotype (referred to as mutants) lack virtually all germ cells. RESULTS: Morphometric determination of Sertoli cell parameters in mutant and control (+/+) animals showed that although the testes of mutant animals were about eight times smaller than controls, the numbers of Sertoli cells in the two groups did not differ. Sertoli cell volume, Sertoli cell cytoplasmic and nuclear volumes, and Sertoli cell surface area in mutant animals were significantly smaller than in control animals. Organelle volumes and surface areas, expressed per cell, did not differ significantly in the two groups with one exception: the volume and surface area of smooth endoplasmic reticulum was significantly reduced in mutant animals. Plasma testosterone levels and tissue testosterone levels/testis were normal, indicating that the effects observed in the mutant animal were not a consequence of androgen insufficiency. Plasma FSH was elevated, probably as a consequence of germ cell depletion, and was thought not to affect Sertoli cell parameters observed. CONCLUSIONS: The data suggest that paracrine interactions with germ cells do affect Sertoli cells by modifying the amount of smooth endoplasmic reticulum. These data focus attention on the function of this abundant Sertoli cell organelle in promoting spermatogenesis.

Animals↗

PubMed1994

Hormone sensitivity of germ cells in stage XIV and in stage I of the rat spermatogenic cycle.

Previous data have been inconclusive with respect to whether the meiotic degenerations that occur in stage XIV of the spermatogenic cycle are increased after hypophysectomy. Meiotic cell degenerations in Stage XIV and early Stage I of the spermatogenic cycle were enumerated to determine if the advanced generation of meiotic cells were influenced by hormonal deprivation subsequent to hypophysectomy and, if so, could cellular degenerations be prevented by supplementation with either testosterone or recombinant FSH during the period of hypophysectomy. The animals utilized were either pituitary-intact rats or rats hypophysectomized for 3 or 10 days. Hormone supplementation began at day 3 post-hypophysectomy and continued until day 10 at which time all animals were sacrificed. The numbers of degenerating meiotic figures (metaphase to telophase of the first and second meiotic division) as expressed per Sertoli cell nucleus or nucleolus were not increased significantly 10 days after hypophysectomy as compared with animals hypophysectomized for 3 days or with pituitary-intact controls. Exogenously administered testosterone and FSH had no effect on the numbers of degenerating meiotic germ cells in hypophysectomized animals. These data indicate that stage XIV metaphase to telophase spermatocytes are not hormone sensitive. However, it was determined that there were new cell types degenerating at Stage XIV and I of the spermatogenic cycle. These were interphase secondary spermatocytes and step 1 spermatids and were seen in stages XIV and I, respectively. These cell degenerations were found in low numbers in Stage XIV and I in either FSH-treated or testosterone-treated rats, suggesting their hormone sensitivity. Thus it is possible that Stages XIV and I are hormone sensitive stages.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

The hamster Sertoli cell in early testicular regression and early recrudescence: a stereological and endocrine study.

Utilizing stereological techniques, the hamster Sertoli cell at Stage VII of the spermatogenic cycle was examined for early signs of regressive changes after short-term photoperiod-induced testicular regression and for early signs of stimulation after short-term photoperiod-induced recrudescence. After 4-6 weeks of exposure to short photoperiod, germ cell degeneration was prominent but there were only minimal changes in Sertoli cell structure. These included a decline in volume of multivesicular bodies and in the surface area of mitochondrial membranes and adluminal plasma membrane, while no changes were noted in the other parameters measured. Of the endocrine changes, only plasma FSH levels had declined at this time and there were virtually no significant correlations between plasma FSH levels and the various structural parameters. The general lack of Sertoli cell changes in response to a short exposure to inhibitory photoperiod in the seasonally breeding hamster is similar to the early response to hypophysectomy in the none-seasonal rat. During early photoperiod-related recrudescence, testis weight, tubular lumen volume and interstitial parameters were increased. Significantly more preleptotene spermatocytes (about a 50% increase) were present in stage VII tubules, though adluminal germ cells did not increase in number. At this time some structural features of the Sertoli cells were enhanced in volume (cytoplasm, smooth and rough endoplasmic reticulum) and surface area (outer and inner mitochondrial membranes, smooth and rough endoplasmic reticulum and the basal compartment plasma membrane). Blood levels of FSH and testosterone were increased significantly but correlated only with rough endoplasmic reticulum, suggesting that initiation of the synthetic processes was important in reestablishment of spermatogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗