3,586 research outputs found

    Gonadotropin and Gonadal Steroid Release in Response to a Gonadotropin-Releasing Hormone Agonist in G_q^ɑ and G_(11)^ɑ Knockout Mice

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    In this study, we used mice lacking the G_(11)^α[ G_(11) knockout (KO)] or G_q^α gene (G_q KO) to examine LH release in response to a metabolically stable GnRH agonist (Buserelin). Mice homozygous for the absence of G_(11)^α and G_q^α appear to breed normally. Treatment of (5 wk old) female KO mice with the GnRH agonist Buserelin (2 μg/100 μl, sc) resulted in a rapid increase of serum LH levels (reaching 328 ± 58 pg/25 μl for G_(11) KO; 739 ± 95 pg/25 μl for G_q KO) at 75 min. Similar treatment of the control strain, 129SvEvTacfBr for G_(11) KO or the heterozygous mice for G_q KO, resulted in an increase in serum LH levels (428 ± 57 pg/25 μl for G_(11) KO; 884 ± 31 pg/25 μl for G_q KO) at 75 min. Both G_(11) KO and G_q KO male mice released LH in response to Buserelin (2 μg/100 μl of vehicle; 363 ± 53 pg/25μ l and 749 ± 50 pg/25 μl 1 h after treatment, respectively). These values were not significantly different from the control strain. In a long-term experiment, Buserelin was administered every 12 h, and LH release was assayed 1 h later. In female G11 KO mice and control strain, serum LH levels reached approximately 500 pg/25 μl within the first hour, then subsided to a steady level (∼100 pg/25 μl) for 109 h. In male G_(11) KO mice and in control strain, elevated LH release lasted for 13 h; however, LH levels in the G_(11) KO male mice did not reach control levels for approximately 49 h. In a similar experimental protocol, the G_q KO male mice released less LH (531 ± 95 pg/25 μl) after 13 h from the start of treatment than the heterozygous male mice (865 ± 57 pg/25 μl), but the female KO mice released more LH (634 ± 56 pg/25 μl) after 1 h from the start of treatment than the heterozygous female mice (346 ± 63 pg/25 μl). However, after the initial LH flare, the LH levels in the heterozygous mice never reached the basal levels achieved by the KO mice. G_(11) KO mice were less sensitive to low doses (5 ng/per animal) of Buserelin than the respective control mice. Male G_(11) KO mice produced more testosterone than the control mice after 1 h of stimulation by 2 μg of Buserelin, whereas there was no significant difference in Buserelin stimulated testosterone levels between G_q KO and heterozygous control mice. There was no significant difference in Buserelin stimulated estradiol production in the female G_q KO mice compared with control groups of mice. However, female G_(11) KO mice produced less estradiol in response to Buserelin (2 μg) compared with control strain. Although there were differences in the dynamics of LH release and steroid production in response to Buserelin treatment compared with control groups of mice, the lack of complete abolition of these processes, such as stimulated LH release, and steroid production, suggests that these G proteins are either not absolutely required or are able to functionally compensate for each other

    Buserelin treatment to rats causes enteric neurodegeneration with moderate effects on CRF-immunoreactive neurons and Enterobacteriaceae in colon, and in acetylcholine-mediated permeability in ileum

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    The gonadotropin-releasing hormone (GnRH) analog buserelin causes enteric neuronal loss. Acute stress or injection of corticotropin-releasing factor (CRF) affects motility, secretion, and barrier function of the gastrointestinal tract. The aim of the study was to characterize the CRF immunoreactivity in enteric neurons after buserelin treatment, and to evaluate possible effects of enteric neuropathy on gut microbiota, intestinal permeability, and stress response behavior

    Effect of goserelin and leuprolide added to the semen on reproductive performance in rabbits — Short communication

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    The aim of this study was to evaluate the ability of two synthetic GnRH analogues, goserelin and leuprolide, to induce ovulation in rabbit does using intravaginal administration. A total of 252 primiparous lactating does were randomly divided into five groups that, at the time of insemination, received the following treatments for ovulation induction: 1 µg of buserelin administered intramuscularly (control group), 5 µg of goserelin added to the semen dose (Group G5), 10 µg of goserelin added to the semen dose (Group G10), 5 µg of leuprolide added to the semen dose (Group L5), and 10 µg of leuprolide added to the semen dose (Group L10). The kindling rate was 80.5% in Group G10 and 75.0% in Group L10; these values are comparable to the kindling rate obtained in the control group (85.9%). The kindling rates in Groups G5 and L5 were significantly lower than in the control group (60.0%, 54.2% and 85.9%, respectively). The number of live-born rabbits was not significantly affected by the ovulation induction treatment. As regards the total number of rabbits born the only significant difference was observed between Groups G5 and L5. This study shows the possibility of inducing ovulation in rabbits by adding goserelin and leuprolide directly to the semen dose
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