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Robert J Norman - One of the best experts on this subject based on the ideXlab platform.

  • effects of leptin administration and feed restriction on thecal leucocytes in the preovulatory rat ovary and the effects of leptin on meiotic maturation granulosa cell proliferation Steroid hormone and pge2 Release in cultured rat ovarian follicles
    Reproduction, 2002
    Co-Authors: Priya S Duggal, Natalie K Ryan, K H Van Der Hoek, Lesley J Ritter, D T Armstrong, Denis A Magoffin, Robert J Norman
    Abstract:

    Leptin is expressed by adipocytes and is thought to play a role in regulating food intake and in reproduction. It has been demonstrated that acute leptin administration to immature gonadotrophin-primed rats in vivo inhibits ovulation and causes a decline in food intake. However, feed restriction alone does not inhibit ovulation. Two experiments were designed to investigate the mechanism of leptin-induced inhibition of ovulation. In the first experiment, which was prompted by the importance of ovarian leucocytes in ovulation, the role of leucocytes in leptin-induced inhibition of ovulation was investigated. The second experiment investigated whether high leptin concentrations could inhibit other factors important to ovulation, such as meiotic competence of oocytes, granulosa cell proliferation, Steroid or PGE(2) Release, and interleukin 1beta production, in vitro. In the first experiment, the populations of neutrophils and monocytes-macrophages in the preovulatory follicles of gonadotrophin-primed, leptin-treated and -untreated rats were examined. A decrease in food intake, as a result of either leptin treatment or feed restriction, specifically reduced the numbers of neutrophils and monocytes-macrophages infiltrating the theca interna of preovulatory follicles without affecting the numbers found in the stroma. The findings show that reduced infiltration of thecal neutrophils and macrophages into preovulatory follicles is a response to reduced food intake. Furthermore, this reduction is not the direct cause of the leptin-induced inhibition of ovulation. In the second experiment, ovarian follicles were cultured for 4 or 12 h in the presence or absence of the following hormones: FSH (500 miu), insulin-like growth factor I (IGF-I) (50 ng ml(-1)), LH (100 ng ml(-1)) and leptin (300 ng ml(-1)). The results demonstrated that high concentrations of leptin in follicle culture do not affect meiotic maturation or Steroid Release, but tend to inhibit Release of PGE 2 (although this result was not significant). DNA synthesis in granulosa cells was not inhibited by leptin in FSH- and IGF-I-supplemented culture media. These results are in agreement with previous studies that have shown that leptin inhibits the stimulatory effects of IGF-I on FSH-stimulated oestradiol production in rat granulosa cells without affecting progesterone production. In summary, leptin does not appear to have an adverse effect on the components of ovulation tested in this study, and therefore must impact on the ovulatory cascade in a way that remains to be defined.

  • inhibition of nitric oxide effects on interleukin 1 beta enhanced ovulation rate Steroid hormones and ovarian leukocyte distribution at ovulation in the rat
    Biology of Reproduction, 1996
    Co-Authors: Nigel Bonello, Kylie Mckie, Melinda J Jasper, Lucy Andrew, Nicki Ross, Emily Braybon, M Brannstrom, Robert J Norman
    Abstract:

    The ovulatory process resembles an inflammatory reaction with an infiltration of leukocytes, production of inflammatory mediators such as cytokines, and a general edema and hyperemia. Nitric oxide (NO), a potent vasodilator and the main mediator of macrophage tumoricidal and bacteriocidal activities, is known to participate in inflammatory reactions and has been shown to mediate the interleukin-1 beta (IL-1 beta)-directed tissue-remodeling events within the ovary. The regulation by NO of ovulation rate, leukocyte distribution, and Steroid Release in the rat ovary was investigated through use of a combination of in vivo and in vitro models of ovulation and a competitive inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), of the NO synthase (NOS) enzyme. Subcutaneous L-NAME (1.5 x 10(-4) mol/kg) administration significantly reduced the in vivo ovulation rate of eCG/hCG-primed rats (L-NAME-treated: 10.6 +/- 1.8 [mean +/- SEM] oocytes per ovary [O/O], 11.0 +/- 1.2 rupture sites per ovary [RS/O]; saline-treated: 18.0 +/- 1.8 O/O, 19.4 +/- 1.1 RS/O; p < 0.01) at 20 h post-hCG. These results were reflected in vitro, where addition of L-NAME (3.5 x 10(-5) mol/L) to LH (0.1 microgram/ml)-perfused ovaries decreased ovulation rate from 8.2 +/- 1.6 to 2.7 +/- 1 ovulations per ovary (p < 0.05) and simultaneously decreased nitrite accumulation at the completion of perfusions from 16.5 +/- 1.9 to 4.1 +/- 0.5 nmol/ml (p < 0.001). The addition of L-NAME to LH+IL-1 beta (4 ng/ml)-perfused ovaries decreased ovulation rate from 15.2 +/- 2.4 to 0.8 +/- 0.8 ovulations per ovary (p < 0.001) and simultaneously decreased nitrite accumulation at 22 h from 22.8 +/- 2.2 to 1.9 +/- 0.6 nmol/ml (p < 0.001). Studies analyzing and manipulating perfusion flow rate indicated that the L-NAME effects on ovulation rate are primarily due to a reduction in flow rate resulting from inhibition of NO, which may be a consequence of the known vasoconstrictor effects of NOS inhibitors. The observed reduction of in vivo ovulation rate by NO inhibition at 20 h post-hCG was associated with a significant reduction in thecal MCA149+ neutrophils at 12 h post-hCG, the expected time of ovulation (L-NAME-treated: 98.4 +/- 9.2 cells per thecal area; saline-treated: 211.5 +/- 11.5 cells per thecal area; p < 0.001), while ED1+ monocytes/macrophages underwent similar but nonsignificant changes. Plasma (20 h post-hCG) and perfusate progesterone were not different with L-NAME treatment, while perfusate estradiol levels were markedly reduced upon addition of L-NAME, suggesting a role for NO in ovulation but not in the process of luteinization. In summary, deprivation of NO by use of the competitive inhibitor, L-NAME, led to fewer ovulations, reduced accumulation of nitrite, a decreased neutrophil count in the theca of preovulatory follicles, and reduced estradiol secretion, while progesterone Release remained unaffected. The NO pathway may therefore play an important role in the regulation of ovulation and the mediation of IL-1 beta's pro-ovulatory effects. There are likely to be primarily vascular effects, but also a nonvascular component, to the NO regulation of ovulation, with both components indirectly affecting ovulatory leukocyte distribution and Steroid secretion.

Victor Viau - One of the best experts on this subject based on the ideXlab platform.

  • central organization of androgen sensitive pathways to the hypothalamic pituitary adrenal axis implications for individual differences in responses to homeostatic threat and predisposition to disease
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2005
    Co-Authors: Martin Williamson, Brenda Bingham, Victor Viau
    Abstract:

    Abstract Despite clear evidence of the potency by which sex Steroids operate on the hypothalamic-pituitary-adrenal (HPA) axis and genuine sex differences in disorders related to HPA dysfunction, the biological significance of this remains largely ignored. Stress-induced increases in circulating glucocorticoid levels serve to meet the metabolic demands of homeostatic threat head-on. Thus, the nature of the stress-adrenal axis is to protect the organism. As one develops, matures, and ages, still newer and competing physiological and environmental demands are encountered. These changing constraints are also met by shifts in sex Steroid Release, placing this class of Steroids beyond the traditional realm of reproductive function. Here we focus on the dose-related and glucocorticoid-interactive nature by which testosterone operates on stress-induced HPA activation. This provides an overview on how to exploit these characteristics towards developing an anatomical framework of testosterone's actions in the brain, and expands upon the idea that centrally projecting arginine vasopressin circuits in the brain act to register and couple testosterone's effects on neuroendocrine and behavioural responses to stress. More generally, the work presented here underscores how a dual adrenal and gonadal systems approach assist in unmasking the bases by which individuals resist or succumb to stress.

  • gender and puberty interact on the stress induced activation of parvocellular neurosecretory neurons and corticotropin releasing hormone messenger ribonucleic acid expression in the rat
    Endocrinology, 2005
    Co-Authors: Victor Viau, Brenda Bingham, Jennifer C Davis, Patricia K Lee, Margaret C Wong
    Abstract:

    Individual variations in hypothalamic-pituitary-adrenal (HPA) function are most evident at or beyond the time of puberty, when marked changes in sex Steroid Release occur. To explore the nature by which gender differences in HPA function emerge we examined in prepubertal (∼30-d-old) and postpubertal (∼60-d-old) male and female rats HPA activity under basal conditions and in response to 30 min of restraint. Within the ACTH-regulating, medial parvocellular portion of the paraventricular nucleus, restraint-induced Fos protein and arginine vasopressin heteronuclear RNA were lower in 60- than in 30-d-old males. No such age-related shift in the response of these synaptic and transcriptional markers of cellular activation occurred in female rats. Basal CRH mRNA expression levels in the paraventricular nucleus increased with age in female but not male rats. Conversely, only male rats showed an age-related increase in basal CRH mRNA in the central amygdala, suggesting that neuronal and neurosecretory CRH-expressin...

Joseph R Sherwin - One of the best experts on this subject based on the ideXlab platform.

  • botulinum c2 toxin and Steroid production in adrenal y 1 cells the role of microfilaments in the toxin induced increase in Steroid Release
    Journal of Pharmacology and Experimental Therapeutics, 1992
    Co-Authors: Robert V Considine, Lance L Simpson, Joseph R Sherwin
    Abstract:

    Exposure of adrenal Y-1 cells to C2 toxin results in an increase in Steroid Release that is accompanied by a rounding of the cell. The actions of C2 toxin mimic those of adrenocorticotropin and cholera toxin except that there is no increase in intracellular cyclic AMP content. In the present study we provide evidence that C2 toxin increases Steroid output from Y-1 cells through an alteration in the microfilament network of the cell. C2 toxin significantly increased Steroid output after 3 hr of exposure. This effect was accompanied by a significant increase in the transport of [3H]cholesterol to the mitochondrial fraction, independent of cholesterol uptake by the cell. The toxin was unable to increase Steroid output from cells prerounded in suspension culture. The protease inhibitors benzamidine and phenylmethylsulfonyl fluoride did not attenuate the ability of C2 toxin to alter the morphology of Y-1 cells. A 3-hr exposure to C2 toxin resulted in the ADP-ribosylation of 50 to 60% of the total actin pool. Fluorescein isothiocyanate-labeled phalloidin visualization of the cytoskeleton of toxin-treated cells confirmed that the toxin caused a decrease in the stress fiber network. C2 toxin treatment of a protein kinase A mutant Y-1 cell (Kin 8) resulted in morphological changes and an increase in Steroid output that was not different from that observed for wild type Y-1 cells. The data suggest that C2 toxin increases Steroid output from adrenal Y-1 cells by a cyclic AMP-independent mechanism that involves the microfilament network of the cell.

Hernan E Lara - One of the best experts on this subject based on the ideXlab platform.

  • participation of vasoactive intestinal polypeptide in ovarian Steroids production during the rat estrous cycle and in the development of estradiol valerate induced polycystic ovary
    Reproduction, 2007
    Co-Authors: Claudio Parra, Jenny L Fiedler, Leticia S Luna, Monika Greiner, Vasantha Padmanabhan, Hernan E Lara
    Abstract:

    Vasoactive intestinal polypeptide (VIP) stimulates estradiol and progesterone Release from ovarian granulosa cells in vitro. Very little information is available as to the role VIP plays in the control of Steroid secretion during reproductive cyclicity and in ovarian pathologies involving altered Steroid secretion. In this study, we determined the involvement of VIP in regulating ovarian androgen and estradiol Release during estrous cyclicity and estradiol valerate (EV)-induced polycystic ovarian development in rats. Our findings show that androgen and estradiol Release from ovaries obtained during different stages of rat estrous cycle mimic cyclic changes in Steroid Release observed in vivo with maximal Release occurring during late proestrus. VIP increased androgen Release from ovaries of all cycle stages except late proestrus and estradiol Release from all cycle stages. Increases in VIP-induced androgen and estradiol Release were maximal at early proestrus. Inclusion of saturating concentrations of androstenedione increased magnitude of VIP-induced estradiol Release at diestrus and estrus but not proestrus. Magnitude of VIP-induced androgen and estradiol Release tended to be greater in the ovaries from EV-treated rats with polycystic ovary compared with estrous controls. At the tissue level, ovarian VIP concentration was cycle stage dependent with highest level seen in diestrus. Maximum concentration of VIP was found in EV-treated rats. Changes in VIP were inversely related to changes in ovarian nerve growth factor, a neuropeptide involved in ovarian androgen secretion. These results strongly suggest that intraovarian VIP participates in the control of estradiol secretion during the rat estrous cycle and possibly in the maintenance of increased ovarian estradiol secretory activity of EV-treated rats.

Jerome M Goldman - One of the best experts on this subject based on the ideXlab platform.

  • Influence of the drinking water disinfection by-product dibromoacetic acid on rat estrous cyclicity and ovarian follicular Steroid Release in vitro.
    Reproductive Toxicology, 2000
    Co-Authors: Sharon K. Balchak, Joan M. Hedge, M.leonard Mole, Ashley S Murr, Jerome M Goldman
    Abstract:

    Abstract The drinking water disinfection by-product, dibromoacetic acid (DBA) has been reported to affect gonadal functions in the male rat. However, there is little information regarding the influence of DBA on female reproductive activity. Consequently, the present study investigated the effects of DBA on estrous cyclicity and the impact in vitro of DBA on ovarian follicular Steroid secretion. Regularly cycling animals were dosed with DBA (0 to 270 mg/kg/day) for 14 days and estrous cyclicity was monitored during treatment and for an additional 2-week posttreatment interval. A dose-related alteration in cyclicity was observed at 90 and 270 mg/kg/day, which persisted through the posttreatment monitoring in the high dose group. An in vitro exposure of preovulatory follicles to DBA was then used to assess the influence of DBA on Steroid Release. To select a concentration for use, a single oral exposure to 270 mg/kg was administered, and the mean blood levels were determined over a 5-h interval. For this in vitro work, pairs of preovulatory follicles from PMSG-primed immature rats were exposed to 0 or 50 μg/mL DBA over a 24-h period and evaluated for estradiol and progesterone Release under baseline and hCG-stimulated conditions. The influence of tumor necrosis factor (TNFα) exposures under these conditions was also determined. In the nonstimulated condition, DBA was found to increase the Release of estradiol, but had no detectable effect in response to hCG. Progesterone, however, showed marked suppression under hCG stimulation following exposure to DBA, while nonstimulated secretion was unaffected. TNFα by itself also suppressed stimulated progesterone Release, but had no additional effect in combination with DBA. The data suggest that one factor in the disruption in estrous cyclicity could be an alteration in Steroid production, which was characterized by separate effects on both estradiol and progesterone secretion.