Junctions between Xenopus laevis oocytes and follicle cells have been identified as gap junctions by the passage of microinjected fluorescent dye from oocytes to follicle cells. The opening or assembly of these junctions, or both, appears to be regulated by gonadotropins.
During development, the oocytes of Xenopus laevis establish junctional contact with the follicle cells enveloping them. These junctions have alternatively been described as desmosomes and as gap junctions. In this paper the morphology of these junctions has been examined in gonadotropin-stimulated and unstimulated animals at all stages of development. Contact between the oocyte and follicle cell plasma membranes is visible in stage I oocytes as thickenings in the membranes, separated by intercellular spaces of 20nm or greater. By stage III in unstimulated oocytes and stage II in gonadotropin-stimulated oocytes, intermembrane spaces at these junctional contacts are often reduced to 2 to 7 nm in width. These narrow intermembrane spaces persist through early stage IV, with greater frequency of occurrence in oocytes taken from hormonally stimulated animals. The closeness of these junctional contacts, and the permeability of the junctional spaces to intercellular tracer substances, supports the evidence that these are gap junctions.
Many postmenopausal women question whether to start or continue hormone therapy because of recent clinical trial negative results. However, evidence from other studies of postmenopausal women, and from studies in menopausal monkeys, indicate that estrogen has neurocognitive protective effects, particularly when therapy is initiated close to the time of menopause before neural systems become increasingly compromised with age. In this review, we present studies of menopausal women and female monkeys that support the concept that estrogen therapies protect both cognitive function and neurobiological processes. Keywords monkeys; hormones; menopause; neurobiology; memoryResults from the Women's Health Initiative Memory Study (WHIMS) [Espeland et al., 2004;Rapp et al., 2003a;Shumaker et al., 2003;Shumaker et al., 2004] has caused many postmenopausal women to question whether to start or to continue hormone therapy (HT) to decrease the risk of developing dementia and has caused many others to question the role of estrogen in protecting cognitive function from age-related decline in general. However, several critical factors likely influenced the WHIMS negative results, including the advanced age of the subjects, delayed timing of HT initiation in relation to when menopause occurred, and the presence of pathological states (e.g., diabetes, hypertension, obesity) [Ancelin and Ritchie, 2005;Genazzani et al., 2007;Maki, 2006;Sherwin, 2005]. In conjunction with the positive results of estrogen obtained in randomized clinical trials in younger women [Sherwin and Henry 2008], multiple factors have led to the development of the "critical period hypothesis" in which it is theorized that estrogen exerts protective effects on cognition only when it is initiated closely in time to menopause, before neural systems become increasingly challenged by age-related changes and/or neurons become less sensitive or responsive to HT.Animal models have proven useful in investigating different parameters of HT neuroprotection in ways that otherwise are not possible in women. Over the last 15 years, our laboratory has used surgically menopausal macaque monkeys as models of postmenopausal women in studies to investigate the neuroprotection by HT of both [Steger and Peluso, 1987], female macaques have 28 day menstrual cycles and patterns of ovarian hormone fluctuations that are similar to those of human females [Goodman et al., 1977;Jewitt and Dukelow, 1972]. These monkeys experience a menopause that closely resembles that of women [Gilardi et al., 1997;Johnson and Kapsalis, 1995], and they also have physiological responses to surgical menopause and estrogen therapy (ET) that are similar to women [Adams et al., 1990;Jayo et al., 1998;Jerome et al., 1994].In the following sections, we present studies of menopausal women and female monkeys that support the concept that estrogen therapies protect both cognitive function and neurobiological processes. Neuroprotection of Cognitive Function Evidence in Postmenopausal WomenSeveral lines of evid...
Se in the form of sodium selenite is toxic to Xenopus laevis embryos and tadpoles continuously exposed to concentrations above 1 ppm. Concentrations of 2 ppm and above result in severe developmental abnormalities and increased mortality. Uptake and loss of radioactive Se from water are rapid, but depuration is not complete indicating that some Se can remain bound by the organism. The facts that Se is toxic at low levels to Xenopus embryos and tadpoles, can cause developmental abnormalities, and accumulates in tissues suggest that increased release of Se compounds into the environment poses a potential threat to aquatic organisms.
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