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Reproductive Ageing (reproductive + ageing)
Selected AbstractsIs Reproductive Ageing Controlled By the Brain?JOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2007Andrea C. Gore Summary Female reproductive function is controlled by complex interactions of the brain, pituitary gland and ovary. Each of these organs produces unique hormones, and each hormone acts upon the other organs to affect a response. Differentiating the causes and the consequences of reproductive senescence in mammals is thus a ,chicken and egg' puzzle. Surprisingly, recent evidence indicates a more important role for the brain in the initiation and transition to reproductive senescence. [source] Alteration in Hypothalamic Neuropeptide Y (NPY) Secretion May Underlie Female Reproductive Ageing: Induction of Steroid-Induced Luteinising Hormone Surge by NPY in Ovariectomised Aged RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006A. Sahu A large body of evidence suggests that a defect in the hypothalamic function may be the primary cause of reproductive ageing in female rats. We have previously shown that luteinising hormone (LH)-surge associated changes in hypothalamic neuropeptide Y (NPY) gene expression and median eminence (ME) NPY levels seen in young rats do not occur in middle-aged (MA) rats. The present study examined whether hypothalamic NPY release is altered during the steroid-induced LH surge in ovariectomised (OVX) MA rats, and whether exogenous NPY initiates steroid-induced LH surge in OVX old rats. In the first study, NPY release from the ME-arcuate nucleus, as assessed by the push,pull cannula technique, was significantly increased before and during the progesterone-induced LH surge in oestrogen (E2)-primed ovariectomised young rats (2,3 months old). This antecedent increase in NPY release seen in young rats was not apparent in MA rats (11,13 months old) in association with a delayed and attenuated LH surge. In the second study, whereas progesterone failed to induce LH surges in E2 -primed ovariectomised old rats (23,25 months old), intracerebroventricular NPY (0.1,0.5 µg) injections at 1100, 1200 and 13.00 h resulted in LH surge induction in E2 + progesterone-primed ovariectomised old rats. Because increased hypothalamic NPY synthesis and release is obligatory for the preovulatory LH discharge in young rats, the present findings suggest that alteration in NPY release from the ME-arcuate nucleus contributes to the delayed and reduced LH surges in MA rats and may be involved in the subsequent loss of the LH surges in old rats. [source] Reproductive ageing in women,THE JOURNAL OF PATHOLOGY, Issue 2 2007O Djahanbakhch Abstract The traditional view in respect to female reproduction is that the number of oocytes at birth is fixed and continuously declines towards the point when no more oocytes are available after menopause. In this review we briefly discuss the embryonic development of female germ cells and ovarian follicles. The ontogeny of the hypothalamic-pituitary-gonadal axis is then discussed, with a focus on pubertal transition and normal ovulatory menstrual cycles during female adult life. Biochemical markers of menopausal transition are briefly examined. We also examine the effects of age on female fertility, the contribution of chromosomal abnormalities of the oocyte to the observed decline in female fertility with age and the possible biological basis for the occurrence of such abnormalities. Finally, we consider the effects of maternal age on obstetric complications and perinatal outcome. New data that have the potential to revolutionize our understanding of mammalian oogenesis and follicular formation, and of the female reproductive ageing process, are also briefly considered. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Male reproductive health research needs and research agenda: Asian and Pacific perspectiveINTERNATIONAL JOURNAL OF ANDROLOGY, Issue S2 2000Yi-Fei Wang Enhancing male reproductive health, and increasing men's participation in it, involves encouraging a range of positive reproductive health and social behaviour by men to help ensure women's and children's well-being. More intellectual work,including research programmes,is urgently needed to clarify the conceptual framework for male reproductive health. At the Asia and the Pacific Symposium ,Intra-regional Cooperation in Reproductive Health Research' (Shanghai, China, 12,13 October 1998) the Symposium participants identified regional research needs and recommended a regional reproductive health research agenda, which addresses six key issues related to male reproductive health: (i) male contraceptive technology; (ii) reproductive tract infections/sexually transmitted diseases and male infertility; (iii) male involvement in reproductive health; (iv) male adolescent reproductive health; (v) male reproductive ageing; and (vi) environment and male reproductive health. One of the major challenges now facing us is the elaboration of a comprehensive, yet realistic, male reproductive health research agenda that reflects the needs and demands of Asian developing countries. Making full use of an interdisciplinary approach is of strategic importance to achieve this. [source] Sex differences in nutrient-dependent reproductive ageingAGING CELL, Issue 3 2009Alexei A. Maklakov Summary Evolutionary theories of aging predict that fitness-related traits, including reproductive performance, will senesce because the strength of selection declines with age. Sexual selection theory predicts, however, that male reproductive performance (especially sexual advertisement) will increase with age. In both bodies of theory, diet should mediate age-dependent changes in reproductive performance. In this study, we show that the sexes exhibit dramatic, qualitative differences in age-dependent reproductive performance trajectories and patterns of reproductive ageing in the cricket Teleogryllus commodus. In females, fecundity peaked early in adulthood and then declined. In contrast, male sexual advertisement increased across the natural lifespan and only declined well beyond the maximum field lifespan. These sex differences were robust to deviations from sex-specific dietary requirements. Our results demonstrate that sexual selection can be at least as important as sex-dependent mortality in shaping the signal of reproductive ageing. [source] Alteration in Hypothalamic Neuropeptide Y (NPY) Secretion May Underlie Female Reproductive Ageing: Induction of Steroid-Induced Luteinising Hormone Surge by NPY in Ovariectomised Aged RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006A. Sahu A large body of evidence suggests that a defect in the hypothalamic function may be the primary cause of reproductive ageing in female rats. We have previously shown that luteinising hormone (LH)-surge associated changes in hypothalamic neuropeptide Y (NPY) gene expression and median eminence (ME) NPY levels seen in young rats do not occur in middle-aged (MA) rats. The present study examined whether hypothalamic NPY release is altered during the steroid-induced LH surge in ovariectomised (OVX) MA rats, and whether exogenous NPY initiates steroid-induced LH surge in OVX old rats. In the first study, NPY release from the ME-arcuate nucleus, as assessed by the push,pull cannula technique, was significantly increased before and during the progesterone-induced LH surge in oestrogen (E2)-primed ovariectomised young rats (2,3 months old). This antecedent increase in NPY release seen in young rats was not apparent in MA rats (11,13 months old) in association with a delayed and attenuated LH surge. In the second study, whereas progesterone failed to induce LH surges in E2 -primed ovariectomised old rats (23,25 months old), intracerebroventricular NPY (0.1,0.5 µg) injections at 1100, 1200 and 13.00 h resulted in LH surge induction in E2 + progesterone-primed ovariectomised old rats. Because increased hypothalamic NPY synthesis and release is obligatory for the preovulatory LH discharge in young rats, the present findings suggest that alteration in NPY release from the ME-arcuate nucleus contributes to the delayed and reduced LH surges in MA rats and may be involved in the subsequent loss of the LH surges in old rats. [source] | ||||||||||