Control Of Oocyte Maturation Research Articles

Concentration of cyclic AMP during the maturation of pig oocytes in vivo and in vitro

Intracellular concentrations of cyclic AMP (cAMP) were measured in pig oocytes maturing in vivo or in vitro. Maturation in vivo was induced with 500 iu hCG administered to gilts treated with pregnant mares' serum gonadotrophin (PMSG). Although PMSG did not affect cAMP concentrations (basal values, 1.69 +/- 0.28 fmol per oocyte), hCG induced a transient rise (8.86 +/- 1.15 fmol per oocyte 12 h after hCG injection). Similarly, the cAMP concentration rose in oocytes maturing in vitro if the oocytes (surrounded or not by cumulus cells) were co-cultured with the follicle wall in the presence of LH. The same increase in cAMP was obtained when denuded oocytes were co-cultured with mural granulosa cells. Theca cells exhibited only a moderate activity, while cumulus cells were totally ineffective. Granulosa cells exposed to LH lost their stimulating influence after 24 h of culture. In the presence of FSH, cAMP production by the oocyte was unaffected by any type of follicle cell. The role of cAMP in the control of oocyte maturation was investigated using dibutyryl cAMP. The presence of dibutyryl cAMP prevented the resumption of meiosis in a dose-dependent manner, but when it was present during the first 12 h of culture only, meiotic progression was accelerated (0 versus 47% of oocytes had germinal vesicles in groups treated with dibutyryl cAMP and control groups, respectively, after 24 h of culture).(ABSTRACT TRUNCATED AT 250 WORDS)

The control of oocyte maturation in the starfish and amphibians by serotonin and its antagonists.

Serotonin acts as antagonist of progesterone on amphibian oocytes. Serotonin antagonists inhibit maturation of starfish oocytes and stimulate or trigger maturation in amphibians. We propose that endogenous serotonin participates in the control of oocyte maturation.

Immunology and Fertility in the Bovine

Antibodies are powerful tools for unlocking normal physiological problems of both qualitative and quantitative nature that affect fertility. In addition, when antibodies are generated due to abnormal situations, fertility is depressed or completely inhibited for varying periods of time. Antibodies to sperm have demonstrated sperm membrane transformations that occur during spermatogenesis and spermiogenesis, the role of the blood-testis barrier, and the role of secretion and absorption in acquisition of sperm fertilizability. Antibodies to ovary have demonstrated factors controlling oocyte maturation, folliculogenesis, and the transudation of macromolecules into the follicle, Fallopian tubes, and uterus that affect capacitation, the acrosome reaction, sperm-oocyte interaction, fertilization, and implantation. Most hormone assays today are immune assays. Antibodies also can purposely suppress fertility (immuno-contraception). Fertility problems can result from inappropriate antibody formation to sperm, oocytes, pregnancy products, or hormones. Fertility problems include auto-immune aspermatogenic orchitis, auto agglutination of sperm, autoimmune oophoritis, allergy to semen or egg yolk semen extenders, isoimmunization of female to sperm, fertilization failure, and embryo mortality due to maternal-fetal incompatibility.

Starfish oocyte maturation: Evidence for a cyclic AMP-dependent inhibitory pathway

Oocyte maturation (meiosis reinitiation) in starfish is induced by the natural hormone 1-methyladenine (1-MeAde). Cyclic AMP seems to play a negative role in maturation since 1-MeAde triggers a decrease of the oocyte cAMP concentration and since intracellular microinjections of cAMP delay or inhibit maturation. Cyclic GMP is also inhibitory but other nucleotides such as cCMP, cIMP, and cUMP are inactive. The involvement of cAMP and cGMP in the control of oocyte maturation has been further investigated by the use of the stereoisomers of the phosphodiesterase-stable adenosine and guanosine 3′,5′-phosphorothioates (cAMPS and cGMPS). The Sp isomers of cAMPS and cGMPS respectively activate cAMP-dependent protein kinase and cGMP-dependent kinase, while the Rp isomers inhibit the kinases. Extracellular addition of these cAMPS and cGMPS isomers has no effect on the oocytes. Intracellular microinjection of the kinase-activating (Sp)-cAMPS and (Sp)-cGMPS delays or inhibits 1-MeAde-induced maturation in a concentration-dependent manner ( I 50, 30 and 300 μ M, respectively). Microinjections of (Rp)-cAMPS and (Rp)-cGMPS have no inhibitory effects and neither trigger nor facilitate maturation. Using various analogs, we found that the delaying or inhibiting effect is restricted to the compounds activating cAMP-dependent kinase, while the compounds inactive on or inhibiting the kinase have no effects on maturation. The inhibitory effect of (Sp)-cAMPS can be reversed by comicroinjection of the heat-stable inhibitor of cAMP-dependent protein kinase, by comicroinjection of the antagonist (Rp)-cAMPS, or by an increase in the 1-MeAde concentration. The negative effects of (Sp)-cAMPS or (Sp)-cGMPS are observed only when these isomers are microinjected during the hormone-dependent period. These results suggest that a cAMP-dependent inhibitory pathway participates in the maintenance of the prophase arrest of oocytes and that 1-MeAde acts both by inhibiting this negative pathway (dis-inhibitory pathway) and by stimulating a parallel activatory pathway leading to oocyte maturation. The generality of this mechanism is discussed.

Role of follicle wall in meiosis reinitiation induced by insulin in Rana pipiens oocytes.

The involvement of the ovarian follicle wall in insulin induction of Rana pipiens oocyte maturation in vitro was examined. Complete removal of the follicle wall significantly decreased, but did not obliterate, oocyte maturation (i.e., germinal vesicle breakdown, GVBD) induced by insulin. Dose-response studies of GVBD induction revealed that oocytes within intact follicles were at least 100 times more sensitive to insulin than denuded oocytes. Addition of cyanoketone, a steroid biosynthesis inhibitor, to intact follicles also suppressed insulin-induced GVBD. Inhibitory effects of either follicle wall removal or cyanoketone were not observed when denuded oocytes were treated with progesterone. Addition of either progesterone or pregnenolone to insulin-treated denuded oocytes augmented the oocyte GVBD response compared to either steroid alone and essentially replaced the effect of the follicle wall. In summary, steroidogenesis in the follicle wall appears to be a major factor contributing to the ability of insulin to induce GVBD. However, whether insulin stimulates follicle wall steroidogenesis or simply augments the biological activity of endogenous basal steroid levels is unresolved. The in vitro results show that oocyte maturation can be modulated by the combined actions of several hormones. Such steroid-insulin interactions may also be relevant to understanding the control of oocyte maturation in amphibians and other vertebrates, including mammals, under physiological conditions in vivo.

In Vitro Oocyte Maturation and Ovulation in Rainbow Trout (Salmo gairdneri), Northern Pike (Esox lucius), and Goldfish (Carassius auratus)

The endocrine processes which control oocyte maturation (resumption of meiosis) and ovulation have been studied in vitro in the trout Salmo gairdneri. Follicular maturation is ultimately under the control of a pituitary gonadotropin which induces the follicle to synthesize specific steroids; these steroids act in turn directly on the oocyte to promote maturation. The systematic study of the in vitro efficiency of various steroids have shown that 17α-hydroxy-20β-dihydroprogesterone plays a preferential role in initiating maturation; this steroid has a high affinity for a plasma protein system. The efficiency of this steroid, similarly to the efficiency of the gonadotropin, can be modulated by other circulating steroids. The precise chronology of some events of follicle maturation have been defined using inhibitors of protein and RNA synthesis.The ovulatory process (sensu stricto: expulsion of matured oocyte from the follicular envelopes) has been experimentally dissociated from oocyte maturation, and some mediators likely to act on ovulation have been identified.These data permit the consideration of novel means of intervention at the ovarian level to synchronize maturation and ovulation in fish, in order to give new tools for progress in aquaculture.

Endocrine control of oocyte maturation and oviducal jelly release in the toad, Bufo bufo (L.).

Abstract An investigation has been carried out into the endocrine control of oocyte maturation and jelly release in the toad. Injection of gravid females with HCG will cause maturation division of the oocytes, ovulation, and release of jelly from the oviducal glands into the oviduct lumen. It has been demonstrated that a progestin released from the ovarian follicles causes both oocyte maturation and jelly release. This conclusion is based on the following results: (a) Jelly release is a response to an ovarian hormone, and oocyte maturation occurs in response to a secretion of the ovarian follicle. (b) Of the different steroids tested, progesterone was the most effective in provoking both oocyte maturation and jelly release. (c) Ovarian influence over both jelly release and oocyte maturation is exerted at least 12 hr before ovulation.