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Biomedical subjects

A Bartke

Publications and source records attributed to A Bartke.

At least 163 records · Page 9Linked to original sources
PubMed1992

Further observations on estrus and ovulation in woodchucks (Marmota monax) in captivity.

The woodchuck is a seasonally breeding sciurid rodent. Female woodchucks are monoestrous and, when isolated from males, remain in a prolonged period of estrus characterized by a clear predominance of cornified cells in the vaginal smear. This study was designed to characterize relationships between the degree of vaginal cornification and sexual receptivity, and to study ovulation and related phenomena of this species in captivity. Fourteen individually caged adult females, maintained under standard laboratory conditions for 9-23 mo, were used in this investigation. Females exhibiting predominantly (67-97%) cornified smears were always receptive, regardless of the time interval from the onset of estrus, and mated within 24 h of pairing. Mated females allowed to complete pregnancy gave birth to live pups 30-32 days later. Litter size ranged from 3-7 pups. Serum progesterone (P) levels increased to approximately 2 ng/ml during the first week of pregnancy and greater than 5 ng/ml during the second and third weeks of pregnancy. Serum estradiol (E2) levels were elevated during the first week of pregnancy and began to decline thereafter. Examination of ovarian serial sections revealed that ovulation took place between 20 and 32 h after copulation. Serum levels increased significantly (4-fold) after ovulation (1.2 +/- 0.3 vs. 0.3 +/- 0.01 ng/ml). However, the circulating levels of E2 remained unchanged between the periods before (53 +/- 1 pg/ml) and after ovulation (60 +/- 3 pg/ml). Ovulation was not simultaneous in all mature follicles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The influence of beta-endorphin on testicular endocrine function in adult rats.

The role of beta-endorphin in testicular steroidogenesis is poorly understood. To address this issue, we treated adult hypophysectomized rats intratesticularly with either saline-50% polyvinylpyrrolidone (SAL-PVP) or human beta-endorphin (0.5 microgram/testis; a total of 1 microgram/rat/day) in SAL-PVP for 3 days. Testicular injections were made under ether anesthesia. On Day 3, rats also received injections (s.c.) of either SAL-PVP or 5 micrograms beta-endorphin in SAL-PVP to minimize the dilution of ether in the testis. One hour later, rats were treated (i.p.) with either saline or ovine LH (25 micrograms/rat). One hour after saline or LH injection, blood was obtained via heart puncture for determination of plasma progesterone (P), androstenedione (A-dione), and testosterone (T) levels. The effects of beta-endorphin (50 ng, equivalent to 13.9 pM; or 250 ng, equivalent to 69.6 pM) on P and androgen secretions in vitro were also examined. Intratesticular injections of beta-endorphin significantly (p less than 0.025) decreased the T response to LH treatment, but failed to affect plasma P and A-dione levels. Response of P to LH treatment was increased (p less than 0.005) in medium containing testicular fragments exposed to 250 ng (69.6 pM) beta-endorphin. However, beta-endorphin attenuated LH effects on A-dione and T production in vitro. These studies demonstrate that beta-endorphin inhibits T secretion, possibly because of its effect on the synthesis of T precursors. Thus, testicular beta-endorphin modulates the endocrine function of the testis in adult rats.

Androgens↗
PubMed1992

Isolation and culture of testicular macrophages from a seasonally breeding species, Phodopus sungorus. Evidence for functional differences between macrophages from active and regressed testes.

We have developed an isolation and cultivation protocol for testicular macrophages from the seasonally breeding Siberian hamster, Phodopus sungorus which allows serum-free culture. Macrophages were isolated from the active testes of adult Phodopus kept in long photoperiod (LD, 18hL:6hD), and from the inactive testes of animals with gonadal regression induced by exposure to a short photoperiod (SD, 6hL;18hD; for 10 weeks). The isolated cells were identified as macrophages by (a) electron microscopy, (b) non-specific phagocytosis, and (c) the presence of Fc-receptors. Treatment of the cultures with oFSH (at 0.5 and 1 micrograms ml-1 for 1 and 4 days) significantly stimulated lactate secretion by testicular macrophages from LD hamsters, as expected from studies in the rat. In marked contrast, oFSH did not affect lactate secretion by testicular macrophages from SD hamsters, or by peritoneal macrophages. To test possible macrophage-Leydig cell interactions, the influence of testicular macrophage-conditioned medium (TM-CM) from FSH-responsive LD macrophage cultures was assessed and compared with the effect of peritoneal macrophage-conditioned medium (PM-CM) on testosterone production by testicular parenchyma from LD hamsters. Unexpectedly, and in contrast to previous reports in rats, testosterone production by testes was inhibited significantly by TM-CM from cultures pretreated with either 0.1 or 0.5 micrograms FSH ml-1. FSH alone stimulated testosterone production (due either to LH contamination or to possible paracrine effects). PM-CM from cultures pretreated with FSH did have an inhibitory effect. It is concluded that: (i) There is indirect evidence for the presence of functional FSH receptors on macrophages from the active testes of Phodopus. (ii) Testicular macrophages from inactive testes of Phodopus are not responsive to FSH, implicating impaired macrophage function in the regressed testes of Phodopus exposed to SD. (iii) Testicular macrophages produce a factor which can inhibit testosterone production by incubated testicular tissue.

Animals↗
PubMed1992

Neuroendocrine function in adult female transgenic mice expressing the human growth hormone gene.

Adult female transgenic mice expressing the human GH (hGH) gene with mouse metallothionein-I promoter are sterile. To evaluate the hypothalamic-pituitary function in these animals, adult female transgenic mice and nontransgenic normal littermates were ovariectomized. On days 7 and 8 after ovariectomy, mice were injected with either oil or primed with 0.5 micrograms estradiol benzoate (EB) in oil, 24 h later treated with 10 micrograms EB/100 g body wt and a day later bled for measurements of FSH, LH, and PRL levels. Plasma gonadotropin and PRL levels were also measured in ovary-intact transgenic and normal siblings at estrus. Additional ovariectomized EB-treated transgenic mice and normal siblings were injected with either saline or GnRH in saline (1 ng/g body wt) and were bled 15 min later for determination of circulating hormone levels. At estrus, in transgenic mice, circulating FSH and PRL levels were significantly lower (FSH:P less than 0.001; PRL:P less than 0.025), but plasma LH concentrations were higher (P less than 0.001) than those in nontransgenic mice. As expected, ovariectomy significantly increased (P less than 0.001) circulating FSH and LH levels in both groups of mice relative to ovary-intact animals, but the increase in plasma LH levels was attenuated in transgenic mice. The suppressive effect of estrogen on circulating FSH and LH levels were similar in transgenic and nontransgenic mice. Treatment with GnRH significantly increased plasma FSH and LH levels in both transgenic and normal mice. However, the plasma FSH and LH responses to GnRH administration were significantly reduced (P less than 0.001) in transgenic mice. The results of these studies indicate that adult female transgenic mice expressing the hGH gene are hypoprolactinemic. Yet due to PRL-like activity of hGH, the gonadotropin secretion is altered. Thus, endogenously secreted hGH modulates the hypothalamic-pituitary function of adult female transgenic mice bearing the hGH gene.

Animals↗
PubMed1992

Structural manifestations of the rat Sertoli cell to hypophysectomy: a correlative morphometric and endocrine study.

Although the Sertoli cell is a key cell mediating the actions of FSH- and LH-stimulated testosterone (T) in the testis, there is little information to indicate how this cell responds structurally to hormonal insufficiency. The present study used morphometric techniques to study the structural manifestations of the Sertoli cell in adult rats hypophysectomized for 6 and 28 days. Six days posthypophysectomy, a period when germ cell degeneration is first evident, tubular diameter and length, testis weights, volume of the interstitium, and volume of most parameters that comprise the interstitium (except blood vessels) showed significant regressive features. However, virtually no parameter relating to the volume and surface area of the Sertoli cell or its subcellular components was significantly reduced compared with that in the normal animal. Thus, at a time when germ cell degeneration is seen in the testis, the Sertoli cell showed no significant structural response to the changing endocrine status of the animal. In contrast, 28 days after hypophysectomy, virtually all parameters relating to the Sertoli cell and its organelles were significantly decreased compared with those in normal animals. Plasma and tissue testosterone, PRL, and FSH showed a very significant decrease 6 days after hypophysectomy compared with intact animals, but at 28 days there was no further significant decrease in the levels of these hormones. There was no correlation of most organelle volumes and surface areas with endocrine parameters. The size of the Sertoli cell showed positive and significant correlations with the volumes and surface areas of all of its cytoplasmic organelles, except the lipid volume. Short term hypophysectomy resulted in no significant change in either the concentration (femtomoles per mg protein) or the content (femtomoles per testis) of FSH receptors, nor was there a significant change in the number of FSH receptors per cell. However, 28 days after hypophysectomy only the content, not the concentration, of FSH receptors decreased significantly along with a decrease in the number of FSH receptors per cell. Although the marked degenerative changes that are seen in the testis 6 days after hypophysectomy parallel endocrine decline, the Sertoli cell responded slowly from a structural standpoint compared with the Leydig cell. After long term hypophysectomy, significant morphometric changes were observed in all of its structural parameters.

Animals↗
PubMed1992

Structural changes in rat Leydig cells posthypophysectomy: a morphometric and endocrine study.

Short and long term responses of the rat Leydig cell were studied posthypophysectomy, at times when germ cell degeneration was first prominent (6 days) and after long term regression of the testis (28 days). In the short term, virtually all structural parameters relating to the volume and surface area of the Leydig cell and its subcellular organelles were significantly lowered compared with those in control animals. Exceptions were the volumes of the nucleolus, heterochromatin, and lysosomes and the surface areas of the nucleus. Structural decreases were generally on the order of 2- to 5-fold in the 6-day period. A statistical analysis of the percent decreases in the short term was performed to determine whether any particular structural features were more sensitive to hypophysectomy than any others. In most instances, no particular organelles were decreased compared to others. However, lipid, although not commonly seen in rat Leydig cells, showed significantly greater percent decreases compared with several other organelles, indicating that the small amount of lipid present is rapidly lost (used) in the short term. After long term hypophysectomy, all structural parameters of the Leydig cell were significantly lowered compared with those in pituitary-intact animals. Only a few parameters (mitochondrial volume, cell surface area, and the surface areas of inner and outer mitochondrial membranes and smooth endoplasmic reticulum) showed more significant decreases in the long term compared with the short term hypophysectomized animals. Most organelle volumes and surface areas correlated positively and significantly with serum and tissue testosterone levels; the exceptions were the volumes of the nucleolus, heterochromatin, lipid, and lysosomes. Compared with the pituitary-intact animal, the content of LH receptors expressed per testis and per Leydig cell was significantly lower in both hypophysectomized groups; however, the number of receptors per given area of individual Leydig cell plasma membrane remained unchanged. Overall, data show that the Leydig cell manifests marked structural changes during early spermatogenic dysfunction.

Animals↗
PubMed1992

Transgenic female mice with high human growth hormone levels are fertile and capable of normal lactation without having been pregnant.

Transgenic mice carrying the phosphoenolpyruvate carboxykinase promoter region-human growth hormone (PEPCK-hGH) fusion gene are characterized by accelerated growth and plasma hGH levels ranging from 100 to 700 ng/ml. Both sexes are fertile, in contrast to previous findings in metallothionein-I/hGH transgenic mice in which females are sterile, apparently due to luteal failure. Virgin transgenic PEPCK/hGH females from this line produce milk and can successfully raise foster litters to weaning. We conclude that the life-long presence of very large amounts of hGH in the circulation is compatible with ovulation, can override the effects of hGH-induced suppression of endogenous PRL release, and can support full lactation in animals that have not been primed by hormonal changes associated with pregnancy.

Animals↗
PubMed1992

Growth response and androgen receptor expression in seminal vesicles from aging transgenic mice expressing human or bovine growth hormone genes.

Previous work has shown that expression of human (h) GH in transgenic mice is associated with significant age-related enlargement of seminal vesicles. To further explore this aberrant growth activity, we have characterized seminal vesicles from various GH transgenic lines and examined their androgen receptor (AR) content and distribution. Six groups of animals were initially studied: young adult (3-5 months) control mice, old (greater than 12 months) control mice, young adult hGH transgenic mice, old hGH transgenics, young adult bovine (b) GH transgenics, and old bGH transgenic mice. Young transgenic mice (hGH and bGH) possessed seminal vesicles with similar relative weights, DNA and protein contents, and AR levels as nontransgenic littermates. Histologically, the glands appeared similar. With aging, the hGH transgenic seminal vesicles exhibited massive stromal hyperplasia, whereas the glands from controls and bGH transgenic mice did not show this response. Seminal vesicles from old hGH mice presented with a marked increase in cell number (DNA content) and a marked decrease in cell size and/or glandular secretions (protein/DNA ratio) compared to those from old controls and young hGH transgenic mice. Tissue AR content was markedly reduced in old hyperplastic hGH seminal vesicles compared to that in seminal vesicles from young hGH transgenics, old controls, and old bGH transgenic mice. Immunohistochemistry indicated the absence of AR in the proliferating stromal cells, whereas acinar epithelial cells showed similar or moderately reduced AR staining intensity compared to control seminal vesicles. To examine whether the above results may be due to insertional mutagenesis rather than hGH itself, two additional GH transgenic lines were examined. Aged transgenic mice expressing bGH with an alternate promoter possessed seminal vesicle weights that were not different from those of old controls, whereas aged transgenic mice expressing an hGH. V gene (variant gene, placental origin) possessed significantly larger vesicles than the controls, which further suggests that vesicular hyperplasia is specifically related to hGH. To assess androgen responsiveness, aged control and hGH transgenic mice were castrated and examined after 15 days. While control seminal vesicles significantly decreased in size, glands from transgenic mice did not. Regressive changes were observed in the remaining epithelium of hGH transgenic mice; however, stromal tissue exhibited no response to androgen withdrawal. The present results suggest that the aging-associated seminal vesicle hyperplasia in hGH transgenic mice is a result of a massive increase in stromal tissue that is low or devoid of AR, suggesting a loss of direct androgen regulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1992

Catecholamines stimulate testicular testosterone release of the immature golden hamster via interaction with alpha- and beta-adrenergic receptors.

Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.

Animals↗
PubMed1992

Effects of age, photoperiod and follicle-stimulating hormone on lactate production by cultured Sertoli cells from prepubertal Siberian hamsters (Phodopus sungorus).

To define a functional difference in Sertoli cells of animals exposed to different photoperiodic conditions, we isolated Sertoli cells from the testes of juvenile Siberian hamsters and cultured them in serum-free medium. In all age groups studied, Sertoli cells isolated from hamsters with delayed and normal puberty responded to follicle-stimulating hormone (FSH) with an increase in lactate production. The increase in lactate production induced by 1000 ng FSH ml-1 was significantly greater in Sertoli cells isolated from hamsters with delayed puberty than in those with normal puberty. These results suggest that Sertoli cells of Siberian hamsters exposed to short photoperiod in vivo may respond to increases in plasma FSH concentrations associated with photostimulation or spontaneous sexual maturation by an increase in secretory activity that may be critical for the initiation of spermatogenesis.

Aging↗
PubMed1992

Effects of expression of human or bovine growth hormone genes on sperm production and male reproductive performance in four lines of transgenic mice.

Reproductive performance was studied in transgenic males from lines expressing and transmitting four hybrid genes: mouse metallothionein-I/human growth hormone (GH) (MT/hGH), MT/hGH placental variant (MT/hGH.V), MT/bovine GH (MT/bGH) and phosphoenolpyruvate carboxykinase/bGH (PEPCK/bGH). Each male was exposed to three normal females for 1 week and to three different normal females for another week. Females were examined for vaginal plugs and necropsied on day 14 of pregnancy. Males were killed for analysis of organ weights, numbers of testicular spermatids, numbers of epididymal sperm and measurements of plasma glucose concentration. Fertility of MT/hGH and MT/hGH.V transgenic males was significantly lower than in normal males, primarily because most males failed to impregnate any females. In females that became pregnant, the numbers of corpora lutea, total fetuses and live fetuses did not differ from those in females mated to normal (nontransgenic) males. Fetal crown-rump length on day 14 of pregnancy did not differ between litters sired by normal or by transgenic males. Weights of testes and seminal vesicles were significantly greater in all four types of transgenic male, but daily sperm production per unit weight (g-1) of testis was not affected and epididymal sperm reserves were either normal or slightly higher than normal. Plasma glucose concentrations were significantly higher in PEPCK/bGH mice than in other mice. Average or individual reproductive performance of transgenic males from the various lines did not correlate with any of the parameters examined except for significantly heavier seminal vesicles in MT/hGH and MT/hGH.V males than in normal males; these transgenic males exhibited a high incidence of infertility. Since hGH and hGH.V, but not bGH, are lactogenic in rodents, it was concluded that chronic stimulation of GH and prolactin receptors by ectopically produced human GHs in transgenic mice compromises male fertility by an unknown mechanism. Reduced fertility of transgenic males with MT/hGH or MT/hGH.V hybrid genes is due to failure to inseminate or impregnate females rather than to reduced numbers of spermatozoa or gross changes in the male reproductive system.

Animals↗
PubMed1992

Differential effects of two alleles of the dy locus on the pituitary-testicular axis of mice.

Testicular function was studied in vivo and in vitro in adult male dy/dy and dy2J/dy2J dystrophic mice. The results demonstrate that testicular function in dy/dy mice is more affected. The basal levels of pituitary hormones measured were normal in dystrophic mice, except for the presence of hyperprolactinemia in dy/dy mice. In dy/dy mice testicular weight was diminished and a deficient transduction of the gonadotropic signal is present in vivo, accompanied by reduced efficiency of 17-hydroxylase and 17-hydroxysteroid dehydrogenase. In dy2J/dy2J mice the signal transduction is normal and the reduction in enzyme efficiency is limited to 17-hydroxysteroid dehydrogenase. The in vitro HCG-induced increases in production of testosterone (T) and estradiol (E2) were reduced in dy/dy/mice, and the data indicate a reduction of enzyme activity rather than in efficiency. In dy21/dy21/mice, HCG-induced T synthesis was increased, HCG-induced E2 synthesis was normal, but basal media E2 levels were reduced, with the in vitro efficiency of aromatase being suppressed under both basal and HCG-stimulated conditions, when compared to their normal littermates.

17-Hydroxysteroid Dehydrogenases↗
PubMed1992

Potentiation by epidermal growth factor of the in vitro HCG stimulation of testicular steroidogenesis in hamsters.

Epidermal Growth Factor (EGF) has been reported to stimulate or inhibit steroidogenesis in murid Leydig cells depending on the experimental conditions used. In the present study, testicular fragments from an adult cricetid rodent, the Syrian hamster, were incubated with various doses of mouse EGF (0-2.0 micrograms/ml media), in the presence or absence of HCG (0-12.5 mlU/ml media). Although EGF alone did not affect in vitro testicular steroidogenesis, it significantly potentiated the HCG-induced elevation of the accumulation of testosterone and 17-hydroxyprogesterone in the media. In contrast, the effect of HCG on media progesterone concentration was not affected by EGF. Since in the Syrian hamster intracellular calcium loading functions as a gonadotropic stimulus, the present results could be a consequence of the EGF-induced increase in cellular calcium levels.

17-alpha-Hydroxyprogesterone↗
PubMed1991

Reinitiation of spermatogenesis by exogenous gonadotropins in a seasonal breeder, the woodchuck (Marmota monax), during gonadal inactivity.

The present study was undertaken (1) to document structural and functional changes in the testes of seasonally breeding woodchuck during active and inactive states of spermatogenesis and (2) to evaluate the ability of exogenous gonadotropins to reinitiate spermatogenesis outside the breeding season. During seasonal gonadal inactivity, there were significant (P less than 0.05) reductions in volumes of several testicular features (testis, seminiferous tubules, tubular lumen, interstitial tissue, individual Leydig cells, Leydig cell nuclei, and Leydig cell cytoplasm) as compared with gonadally active animals. The diameter of the seminiferous tubules was decreased by 26%, and Leydig cell numbers also declined in the regressed testes. These changes were accompanied by a decline in testosterone (T) levels in both plasma and testis, and reduction in epithelial height of accessory reproductive organs. A hormonal regimen was developed that would reinitiate spermatogenesis in captive, sexually quiescent woodchucks. A combination of PMSG and hCG markedly stimulated testicular growth and function and restored spermatogenesis qualitatively. Quantitatively normal spermatogenesis was restored in 2 of 6 treated males. Morphometric analyses revealed substantial increases in seminiferous tubular diameter and in the volume of seminiferous tubules, tubular lumen, total Leydig cells, and individual Leydig cells in the hormone-treated animals. These increased values corresponded to 99, 75, 68, 51, and 200%, respectively, of the values measured in naturally active woodchucks. Leydig cell numbers, however, remained unchanged and approximated only 31% of the number found in naturally active testes. Hormonal stimulation also resulted in a significant rise in serum T as well as in the total content of testicular T, and a marked increase in epithelial height in various accessory reproductive glands. The most effective hormonal protocol for stimulating spermatogenesis was treatment with 12.5 IU of PMSG twice a week for 4 weeks followed by 12.5 IU of PMSG + 25 IU of hCG twice a week for 4 weeks.

Animals↗
PubMed1991

Effect of photoperiod on the rate of 3H-thymidine incorporation of epididymal principal cells in adult Syrian hamsters.

Photoperiod-induced cycles of gonadal regression and recrudescence in the Syrian hamster were used to determine if epididymal growth in adults involves mitotic activity of principal cells. In Experiment 1, the following groups of adult hamsters were examined: induced recrudescing (5L:19D [5 hr light and 19 hr dark] for 13 wk followed by 14L:10D for at least 3 wk), spontaneous recrudescing (5L:19D for 25 wk), and active gonadal state (14:10D). In Experiment 2, adult hamsters were divided into the following groups: induced recrudescing, active, and regressed (5L:19D for 16 wk). Hamsters received subcutaneous injections of 0.5 microCi 3H-thymidine/g body weight three times/wk for 3 wk. The epididymis was fixed in a glutaraldehyde followed by osmium, embedded in Epon 812, and sectioned at 1 micron. Slides were dipped in Kodak NTB-3 emulsion, exposed for 2 or 3 months, developed, and evaluated for isotopic labeling of principal and basal cell nuclei by scoring 500 to 1,000 nuclei. In Experiment 1, the percentages of labeled principal cell nuclei for the induced recrudescing, spontaneous recrudescing, and active groups were 26 +/- 2%, 23 +/- 5%, and 9 +/- 1%, respectively. Considering the intermittent availability of 3H-thymidine during 21 days, this represents daily recruitment of 6.3%, 5.6%, and 2.2%, respectively. In Experiment 2, the percentages of labeled principal cell nuclei for induced recrudescing, active, and regressed groups were 12 +/- 4%, 3 +/- 1%, and 4 +/- 1%, respectively. There was no effect of photoperiod on labeling pattern of basal cells (1.5 +/- 0.6%, 1.2 +/- 0.1%, 0.4 +/- 0.1% for the three photoperiod groups, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Seasonal variations in circulating levels of progesterone and estradiol in unmated adult female woodchucks (Marmota monax) in captivity.

The annual profile of serum levels of progesterone (P) and estradiol-17 beta (E2) was characterized in a seasonally breeding rodent, the woodchuck (Marmota monax). Hormonal levels were determined in serum samples taken at weekly or biweekly intervals from unmated female woodchucks maintained all year indoors under controlled conditions of photoperiod and temperature. Annual fluctuations included a rise of E2 levels during late January through February, followed by a modest increase in plasma P concentrations by late March, the latter attaining peak values during April and May. A temporal dissociation of peak values of circulating levels of P and E2 during the annual reproductive cycle was also detected. The timing of changes in serum levels of P and E2 in these captive woodchucks corresponded to reproductive events during the normal breeding season of the woodchuck in the southern part of its range.

Animals↗
PubMed1991

Cyclic adenosine monophosphate (cAMP) does not mediate the stimulatory action of norepinephrine on testosterone production by the testis of the golden hamster.

The role of cAMP in mediating the stimulatory effects of norepinephrine (NE) on testosterone (T) production by hamster testes in vitro was examined using tissue from both gonadally active and gonadally regressed hamsters. As expected from our previous studies, the NE-induced increase in T accumulation in this system was prevented by alpha-adrenoreceptor antagonist prazosin, but not by beta-adrenoreceptor antagonist propranolol. In incubations of regressed testes from short photoperiod-exposed hamsters, NE stimulated accumulation of cAMP in media and tissue. These effects were prevented by propranolol but not by prazosin. In incubations of active testes from long photoperiod-exposed animals, NE stimulated cAMP in the media but not in the tissue, and potentiated the effect of hCG on the accumulation of cAMP only in tissue. When added to incubations with NE and hCG, propranolol, but not prazosin, reduced cAMP levels in media and tissue. Thus, functional alpha- and beta-adrenoreceptors are present in active and regressed testes and can be activated by NE. NE stimulates cAMP production via its action at the beta-receptors and T production via its action at the alpha-receptors. These results imply that cAMP does not mediate the stimulatory action of NE on T production in hamster testes.

Animals↗