Biomedical subjects

A Mayerhofer

Publications and source records attributed to A Mayerhofer.

82 records · Page 5Linked to original sources

PubMed1989

Catecholamine effects on testicular testosterone production in the gonadally active and the gonadally regressed adult golden hamster.

Several lines of evidence support a role of testicular innervation and peripheral catecholamines in the control of male gonadal function, particularly before puberty. It was therefore of interest to compare the effects of catecholamines on androgen production during the periods of gonadal activity and quiescence in a seasonally breeding species. We have examined direct effects of epinephrine (EPI), norepinephrine (NE), the beta-adrenergic agonist isoproterenol (ISO), and the alpha-adrenergic agonist phenylephrine (PHE) on testicular testosterone (T) production in hamsters with gonadal regression induced by 12 wk exposure to short photoperiod (SD) and in gonadally active hamsters maintained in long photoperiod (LD). Fragments of decapsulated testes were incubated with various combinations of these catecholamines (10(-5)-10(-9) M), human chorionic gonadotropin (hCG; 3.1 mIU/ml), the beta-receptor antagonist propranolol (10(-5) M) and the alpha-l-receptor antagonist prazosin (10(-5) M), for 6 h. In the incubations of testes from LD hamsters, the accumulation of T in the medium was stimulated by hCG but not affected by either catecholamine. However, EPI, NE, and PHE at 10(-5) M, but not ISO, augmented the stimulation of T by hCG. In sharp contrast to these findings, T production by the regressed testes of SD animals was stimulated by EPI (at 10(-8)-10(-5) M), NE (at 10(-6)-10(-5) M), and PHE (at 10(-6)-10(-5) M) in a dose-related manner, but unaffected by ISO. These stimulatory effects were prevented by prazosin, but not by propranolol. Moreover, 10(-5) M of EPI, NE, and PHE augmented the stimulatory effect of hCG on T production. We conclude that the seasonal transition from gonadal activity to quiescence in the adult golden hamster is accompanied by a major increase in the responsiveness of testicular steroidogenesis to catecholamines acting via the alpha-1-adrenoreceptor and that catecholamines can modulate Leydig cell response to gonadotropins in this species. These findings could be related to up-regulation of the alpha-1-receptor in the testis of the SD animal and suggest that catecholamines may be involved in the regulation of the testis during physiological suppression of gonadotropin release and during stress.

Animals↗

PubMed1989

Histamine affects testicular steroid production in the golden hamster.

Localization of mast cells in the testis and ability of histamine (HA) to stimulate testicular testosterone (T) production in vitro were examined in gonadally active adult golden hamsters, kept under a long daily photoperiod (LD) and in gonadally regressed adult golden hamsters exposed to an inhibitory short photoperiod (SD). In both groups mast cells were present in the capsule of the testes and occasionally in vicinity of intratesticular blood vessels. Histamine stimulated T production in a dose dependent manner in incubations of regressed testes of SD animals, but had no stimulatory effect in the active testes of LD animals. In the incubations of SD testes, the effects of HA were abolished by the H-1 antagonist pyrilamine, but unaffected by the H-2 antagonist cimetidine. In both groups, HA enhanced the stimulatory effects of hCG. These results indicate that HA has steroidogenic activity in the testis and may be a factor involved in the regulation of Leydig cell function.

Animals↗

PubMed1989

Histamine affects testicular steroid production in the golden hamster.

Animals↗

PubMed1989

Chronic administration of a gonadotropin-releasing hormone (GnRH) agonist affects testicular microvasculature.

Three months of daily sc injections of adult male dogs with the gonadotropin-releasing hormone agonist (GnRH-A) [D-Trp6, des-Gly-NH2(10)]GnRH ethylamide produced significant decrease in the diameter of seminiferous tubules and conspicuously altered the ultrastructure of testicular microvasculature. In contrast to capillaries and venules in untreated controls, which had typical continuous endothelial layers surrounded by a basal lamina, in testes of dogs chronically treated with GnRH-A, 14.3% of the capillaries and 21.2% of the venules showed wide (30-500 nm) endothelial gaps. In a few capillaries (1.7%) and venules (4%) endothelial fenestrations were found. A high percentage of capillaries (59.3%) and venules (32.8%), with endothelial gaps or continuous endothelium were surrounded by multiple layers of basal lamina. All arterioles, 24.7% of the capillaries and 42.6% of the venules showed the normal features as found in the controls. Superfluous basal laminae, not associated with cells were present in the testes of the chronically treated dogs, but were also found after 4 months of recovery from the GnRH-A treatment. However, within 4 months after cessation of the GnRH-A treatment, the diameters of the seminiferous tubules were comparable to those in untreated controls. Capillaries and venules with endothelial gaps or fenestrations were completely absent. All arterioles, 43.6% of the capillaries and 65.6% of the venules revealed the normal features of continuous endothelium. However, 56.4% of the capillaries and 34.4% of the venules were characterized by superfluous layers of basal lamina.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Formation and regression of capillary sprouts in corpora lutea of immature superstimulated golden hamsters.

The ultrastructure of developing and regressing capillary sprouts was studied in corpora lutea of immature golden hamsters between days 4 and 7 after the application of serum gonadotrophin of pregnant mares (PMSG). Horseradish peroxidase (HRP), an endothelial tracer, was localized by ultrahistochemistry. The vascular permeability of HRP was quantified by an enzyme assay in ovarian homogenates. Sprouting endothelial cells looked activated. They showed micropinocytotic vesicles in a high endothelium surrounded by basal laminae. Early capillary growth was at its maximum on day 4 after PMSG. Advanced capillary growth was seen on days 4 and 5 after PMSG. The vascular lumina were formed by dilatation of the interendothelial space. Regression of capillary sprouts started on day 5, was most intense on day 6 and negligible on day 7. Two processes of regression were observed. One led to a complete destruction, the other to an incomplete one. Vascular permeability decreased between days 5 and 6 after PMSG. It is concluded that the corpus luteum can be viewed as a physiological model of angiogenesis.

Animals↗

PubMedDate not supplied

Ultrastructural aspects of the goiter in cog/cog mice.

Thyroids of congenitally goitrous (cog/cog) mice were studied with light and electron microscopy. The principal alteration in follicular cells was their largely overdistended rough endoplasmic reticulum (RER). Our findings resemble the ultrastructural features of human hypothyroid goiter caused by a thyroglobulin (TG) defect and thus support the previously suggested abnormalities of TG synthesis and/or processing in cog/cog mice.

Animals↗

PubMedDate not supplied

Evidence for catecholaminergic, neuronlike cells in the adult human testis: changes associated with testicular pathologies.

Neuronlike, catecholaminergic cells expressing tyrosine-hydroxylase (TH) have recently been found in the testis of a nonhuman primate species, the rhesus monkey. We examined whether neuronlike cells are present in the human testis. To this end, we first determined if the genes for TH and for a voltage-activated sodium channel (NaCh), a prerequisite for neuronal excitability, are expressed in normal adult testes. Using an RT-PCR approach, cDNA clones, identical to the sequences of human TH and to the alpha subunit of a NaCh type, were isolated. Immunohistochemical methods localized the corresponding proteins in testicular biopsies from adult men (age range, 28-44 years) without testicular pathologies and from infertile patients with either Sertoli cell only (SCO) syndrome or severe hypospermatogenesis and germ cell arrest (GA). TH and NaCh antibodies, as well as antibodies recognizing dopamine-transporter protein, identified immunoreactive cells of mainly bipolar or occasionally multipolar, elongated phenotype in most, but not all, biopsies of each group (12 out of 23). The results were corroborated by identification of TH gene expression by RT-PCR approaches in biopsies. Immunoreactive cell bodies, as well as nerve fibers, were more readily detected in SCO and GA biopsies. This was quantified after immunohistochemically visualizing all testicular neuronal elements, cell bodies, and fibers, with a neurofilament 200 (NF-200) monoclonal antibody in one set of randomly selected sections from all biopsies. We found significantly increased NF-200-immunoreactive cell bodies and fibers in SCO-syndrome and GA biopsies. These results show the existence of an as yet unknown testicular catecholaminergic neuronlike cell type in the human testis. This cell type may complement and act in concert with the well-known testicular sympathetic innervation. The increase of both "intrinsic" (neuronal cells) and "extrinsic" (nerve fibers) neuronal elements in pathological testicular biopsies suggests that the two parts of the human testicular nervous system may be involved in pathogenesis and/or maintenance of GA and SCO syndromes.

Adult↗

PubMedDate not supplied

Pituitary-testicular axis in cardiomyopathic Syrian hamsters.

Testicular function and other endocrine parameters were studied in cardiomyopathic hamsters. In these animals, the major defect is an intracellular calcium overload, which is due to defective voltage-sensitive calcium channels. Basal circulating gonadotropin, prolactin, and triiodothyronine levels were lower in cardiomyopathic hamsters than in normal hamsters, but thyroxine, progesterone, and testosterone levels were not. In cardiomyopathic hamsters, the luteinizing hormone receptor (LHR) positive autoregulation by human chorionic gonadotropin (hCG) reached a maximum faster and at a lower dose than in normal hamsters. Similar results were observed for the response of circulating testosterone to hCG administration. The data indicate that, in spite of deficient pituitary function, cardiomyopathic hamsters have a normal or more efficient testicular function. This is probably the result of the cellular calcium overload, which would stimulate Leydig cell gene transcription, specifically that for LHR.

Animals↗

PubMedDate not supplied

Testicular function after local injection of 6-hydroxydopamine or norepinephrine in the golden hamster (Mesocricetus auratus).

Although there is evidence for the sympathetic innervation of the mammalian testis, the function of noradrenergic fibers is not understood. This in vivo and in vitro study in the adult golden hamster examines testicular function after unilateral intratesticular application of a single dose of 6-hydroxydopamine (6-OHDA), a neurotoxic drug known to produce depletion of noradrenergic stores in nerve endings. The contralateral testis in each animal was injected with vehicle alone and served as the control. After 24 h, the content of norepinephrine (NE) in testicular parenchyma was reduced in most testes injected with 6-OHDA. At this time, concentration of luteinizing hormone receptors (LH-R) was significantly decreased in the 6-OHDA treated testis, compared with the vehicle-injected testes. This decrease was followed by a significant increase at 72 h. The concentration of LH-R was not significantly altered 10, 48, 144, or 168 h after 6-OHDA administration. Changes in testicular testosterone (T) concentrations paralleled the changes in LH-R at most time points. In the incubations of control vehicle injected testes, addition of NE did not affect T production but stimulatory action of hCG was significantly augmented by concomitant exposure to NE at most time points after injection of vehicle. In incubations of 6-OHDA-injected testes, a comparable pattern of T responses to NE and hCG was found only 48 h after injection. At 24 h post injection NE alone significantly stimulated T production; at 10 and 24 h the ability of NE to potentiate the action of hCG was significantly reduced, while at 72 and 144 h basal T production and the stimulatory hCG effect were significantly increased. Moreover, at 72, 144, and 168 h, the effect of NE & hCG on T production was significantly greater in 6-OHDA-injected testes than in the vehicle injected testes of the same animals. In incubations of untreated hamster testes, addition of 6-OHDA at doses similar to those used for injections did not affect T production. Weights of 6-OHDA injected testes were slightly but significantly reduced after 144 and 168 h. These changes were most likely due to degenerative changes of the germinal epithelium, which were clearly detectable 168 h post injection. Because 6-OHDA can release NE from nerve terminals, the observed effects of 6-OHDA might have been initiated by supernormal testicular NE concentrations. To examine this possibility, the authors have tested the effects of intratesticular NE injections. This treatment caused decrease of LH-R at 24 h followed by an increase at 72 h.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗

PubMedDate not supplied

The neural cell adhesion molecule (NCAM) provides clues to the development of testicular Leydig cells.

As previously shown, Leydig cells in culture dramatically up-regulate the expression of the neural cell adhesion molecule (NCAM) gene and express alternatively spliced forms. Because the family of NCAM adhesion molecules is known to be involved in cell migration and differentiation, we examined the potential involvement of NCAMs in Leydig cell differentiation in the developing testis. We detected NCAM-immunoreactive cells in the rat and mouse at embryonic day (ED) 13-14 in epithelia of mesonephric tubules and cell clusters between the mesonephros and testis. At about ED 17-18, strongly NCAM-immunoreactive cells were demonstrated extending from the mesonephros/mesonephric tubules into the region occupied by the forming rete testis and spreading into the testis itself. Within the testis, interstitial fetal Leydig cells, identified with an antiserum directed against P450-side-chain cleavage enzyme, were also NCAM immunoreactive, although to a lesser degree, and in part expressed NCAM-associated polysialic acid. In situ hybridization histochemistry demonstrated the presence of NCAM mRNA, mainly in the cell population corresponding to the strongly immunoreactive cells. NCAM forms with molecular weights of 140 and 180 kDa, the latter polysialylated, predominate in immunoblots of fetal testes. Because testicular development occurs along the mesonephros, from which precursor cells are thought to migrate into the developing gonad and then differentiate into the various testicular cell types, our results may suggest that the expression of NCAMs and NCAM modification are associated with cells that appear to migrate into the developing testis. Although it remains to be proven whether these cells could be precursor cells of Leydig cells, this assumption is supported by the fact that within the developing testis, NCAMs and NCAM modifications are expressed during differentiation of testicular P450-side-chain cleavage enzyme-positive Leydig cells. Thus, the adhesion molecule NCAM and its variants and modifications are expressed in the developing testis and may be of functional, "morphogenic" importance. Because Leydig cells in vitro and during fetal development express NCAMs, these molecules may prove to be a suitable specific marker for the study of Leydig cell development and differentiation.

Animals↗