Egg quality of an Asian catfish of the Mekong river (Pangasius hypophthalmus) during the process of maturation induced by hCG injections

In captive Pangasius hypophthalmus, oocyte maturation and ovulation are induced by hormonal injection following a given protocol: preparatory injections (500 VI.kg-) and decisive injection (2000 VI.kg-). The aim ofthis work is to specify the timing of ovulation and the effects of varying latency period on the quality of ova. Oocytes and ova were collected by intra-ovarian biopsy and hand stripping. Ova quality was estimated by fertilisation rate, hatching rate and proportion of deformed larvae. Ovulation occurred as a synchronous process 8h30 to 9h30 after the last hormonal injection. The first ova obtained (8h30 after injection) were of good quality (85% hatching). At this time, the ovulation rate was 100010. Three hours after ovulation, ageing of ova started to occur: the proportion of deformed larvae increased (24%) and hatching rate collapsed (35%). In P. hypophthalmus, the optimised latency period was found to be 8h30 and corresponded approximately to the completion of ovulation

Short oestrous cycles in sheep during anoestrus involve defects in progesterone biosynthesis and luteal neovascularisation

Anoestrous ewes can be induced to ovulate by the socio-sexual, 'ram effect'. However, in some ewes the induced ovulation is followed by an abnormally short luteal phase causing a so called, "short cycle". The defect responsible for this luteal dysfunction has not been identified. In this experiment we investigated ovarian and uterine factors implicated in male-induced short cycles in anoestrus ewes using a combined endocrine and molecular strategy. Prior to ovulation, we were able to detect a moderate loss of thecal expression of steroid acute regulatory protein (STAR) in ewes that had not received progesterone priming (which prevents short cycles). At and following ovulation we were able to identify significant loss of expression of genes coding key proteins involved in the biosynthesis of progesterone (STAR, CYP11A1, HSD3B) as well as genes coding proteins critical for vascular development during early luteal development (VEGFA, VEGFR2) suggesting dysfunction in at least two pathways critical for normal luteal function. Furthermore, these changes were associated with a significant reduction of progesterone production and luteal weight. Additionally, we cast doubt on the proposed uterine-mediated effect of prostaglandin F2α as a cause of short cycles by demonstrating both the dysregulation of luteal expression of the PGF receptor, which mediates the luteal effects of PGF2α, and by finding no significant changes in the circulating concentrations of PGFM, the principal metabolite of PGF2α in ewes with short cycles. This study is the first of its kind to examine concurrently, the endocrine and molecular events in the follicular and early luteal stages of the short cycle

The "Ram Effect": A "Non-Classical" Mechanism for Inducing LH Surges in Sheep

During spring sheep do not normally ovulate but exposure to a ram can induce ovulation. In some ewes an LH surge is induced immediately after exposure to a ram thus raising questions about the control of this precocious LH surge. Our first aim was to determine the plasma concentrations of oestradiol (E2) E2 in anoestrous ewes before and after the "ram effect" in ewes that had a "precocious" LH surge (starting within 6 hours), a "normal" surge (between 6 and 28h) and "late» surge (not detected by 56h). In another experiment we tested if a small increase in circulating E2 could induce an LH surge in anoestrus ewes. The concentration of E2 significantly was not different at the time of ram introduction among ewes with the three types of LH surge. "Precocious" LH surges were not preceded by a large increase in E2 unlike "normal" surges and small elevations of circulating E2 alone were unable to induce LH surges. These results show that the "precocious" LH surge was not the result of E2 positive feedback. Our second aim was to test if noradrenaline (NA) is involved in the LH response to the "ram effect". Using double labelling for Fos and tyrosine hydroxylase (TH) we showed that exposure of anoestrous ewes to a ram induced a higher density of cells positive for both in the A1 nucleus and the Locus Coeruleus complex compared to unstimulated controls. Finally, the administration by retrodialysis into the preoptic area, of NA increased the proportion of ewes with an LH response to ram odor whereas treatment with the α1 antagonist Prazosin decreased the LH pulse frequency and amplitude induced by a sexually active ram. Collectively these results suggest that in anoestrous ewes NA is involved in ram-induced LH secretion as observed in other induced ovulators

Inflammation is a key contributor to ovarian cancer cell seeding.

The incidence of ovarian cancer dramatically increases in early menopause but the factors contributing to cancer onset are unclear. Most ovarian cancers originate in the fallopian tube with subsequent implantation of malignant cells into the ovary. However, the events and conditions that lead to cancer cell implantation are unknown. To quantify which conditions are conducive to the seeding of cancer cells in an immunocompetent mouse model, we surgically implanted mouse ovarian cancer cells into the oviducts of syngeneic mice and simulated conditions associated with ovulatory wound repair, incessant ovulation, ovarian surface scarring, and aging. We found that the dominant site of cancer cell seeding was not the ovary but the nearby surgical wound site, which was associated with a strong and persistent inflammatory reaction. Conditions in the ovary associated with inflammation, such as acute ovulatory wound repair, active healing of the scarred ovarian surface, and mouse aging, contributed to increased seeding of the cancer cells to the surgical wound site and tissues surrounding the ovary. Changes in the ovary not accompanied by inflammation, such as completed ovulatory cycles and fully-healed scars on the ovarian surface, did not contribute to increased cancer cell seeding. We conclude that inflammation is the most likely mechanism by which ovulation and postmenopausal events contribute to the increased risk of ovarian cancer

Estrous behavior in dairy cows: identification of underlying mechanisms and gene functions

Selection in dairy cattle for a higher milk yield has coincided with declined fertility. One of the factors is reduced expression of estrous behavior. Changes in systems that regulate the estrous behavior could be manifested by altered gene expression. This literature review describes the current knowledge on mechanisms and genes involved in the regulation of estrous behavior. The endocrinological regulation of the estrous cycle in dairy cows is well described. Estradiol (E2) is assumed to be the key regulator that synchronizes endocrine and behavioral events. Other pivotal hormones are, for example, progesterone, gonadotropin releasing hormone and insulin-like growth factor-1. Interactions between the latter and E2 may play a role in the unfavorable effects of milk yield-related metabolic stress on fertility in high milk-producing dairy cows. However, a clear understanding of how endocrine mechanisms are tied to estrous behavior in cows is only starting to emerge. Recent studies on gene expression and signaling pathways in rodents and other animals contribute to our understanding of genes and mechanisms involved in estrous behavior. Studies in rodents, for example, show that estrogen-induced gene expression in specific brain areas such as the hypothalamus play an important role. Through these estrogen-induced gene expressions, E2 alters the functioning of neuronal networks that underlie estrous behavior, by affecting dendritic connections between cells, receptor populations and neurotransmitter releases. To improve the understanding of complex biological networks, like estrus regulation, and to deal with the increasing amount of genomic information that becomes available, mathematical models can be helpful. Systems biology combines physiological and genomic data with mathematical modeling. Possible applications of systems biology approaches in the field of female fertility and estrous behavior are discusse

Peripheral and central mechanisms involved in hormonal control of male and female reproduction

Reproduction involves the integration of hormonal signals acting across multiple systems togenerate a synchronized physiological output. A critical component of reproduction is the luteinizinghormone (LH) surge, which is mediated by estradiol (E2) and neuroprogesterone interacting tostimulate kisspeptin release in the rostral periventricular nucleus of the third ventricle in rats. Recentevidence has shown that both classical and membrane E2 and progesterone signaling is involved inthis pathway. A metabolite of gonadotropin-releasing hormone (GnRH), GnRH-(1-5), has been shownto stimulate GnRH expression, secretion, and has a role in the regulation of lordosis. Additionally,gonadotropin-inhibitory hormone (GnIH) projects to and influences the activity of GnRH neurons inbirds. Stress-induced changes in GnIH have been shown to alter breeding behaviors in birds,demonstrating another molecular control of reproduction. Peripherally, paracrine and autocrineactions within the gonad have been suggested as therapeutic targets for infertility in both males andfemales. Dysfunction of testicular prostaglandin synthesis is a possible cause of idiopathic maleinfertility. Indeed, local production of melatonin and corticotropin-releasing hormone (CRH) couldinfluence spermatogenesis via immune pathways in the gonad. In females, vascular endothelialgrowth factor A (VEGF-A) has been implicated in an angiogenic process that mediates developmentof the corpus luteum and thus fertility via the Notch signaling pathway. Age-induced decreases infertility involve ovarian kisspeptin and its regulation of ovarian sympathetic innervation. Finally,morphological changes in the arcuate nucleus of the hypothalamus influence female sexualreceptivity in rats. The processes mediating these morphological changes have been shown toinvolve rapid effects of E2 controlling synaptogenesis in this hypothalamic nucleus. Together, thisreview highlights new research in these areas, focusing on recent findings in the molecularmechanisms of central and peripheral hormonal control of reproduction.Fil: Rudolph, L. M.. University of California at Los Angeles; Estados UnidosFil: Bentley, G. E.. University of California Berkeley; Estados UnidosFil: Calandra, Ricardo Saul. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Paredes, A. H.. Universidad de Chile; ChileFil: Tesone, Marta. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Wu, T. J.. Uniformed Services University; Estados UnidosFil: Micevych, P. E.. University of California at Los Angeles; Estados Unido

Rodent Models of Polycystic Ovary Syndrome

Rodents are clearly valuable models for assessing disruption of fertility. The effects of different steroid treatments at different stages of reproductive life through from fetal to adult have been assessed for effects on fertility, ovarian morphology, hypothalamic- pituitary function or metabolic consequences. The results show that steroid treatments do disrupt fertility in many cases, but the underlying mechanisms are complicated by the effects of the different treatments at multiple sites. As models for PCOS at the ovarian level however, there are a number of problems particularly related to the fact that rodents are multi-ovular species. Apart from an absence of ovulation and corpora lutea, many of the different steroid regimes result in an increase in large atretic, or cystic follicles that do not parallel PCOS in women. Indeed a number of treatments are given at times when they will cause disruption of the positive feedback effects of estradiol, thus blocking ovulation in adult life. The resulting ovarian morphology thus appears to be like that of PCOS but is in fact not a clear mimic. This review of the various studies highlights parallels and problems with the use of rodents to study the mechanisms underlying the development of PCOS in women