Age-related neurodegenerative changes in the central nervous system of estrogen-deficient follitropin receptor knockout mice

Age-related neurodegenerative conditions are characterized by neuronal death and degeneration that lead to a progressive functional decline. Among the factors influencing degenerative processes during aging are altered levels of neurotrophic ovarian steroid 17beta-estradiol (E2). The follitropin receptor knockout (FORKO) female mouse displays hormonal imbalance characterized by very low levels of circulating E2 and high levels of testosterone. FORKO mice (24 days and 20 months) were used to investigate structural and functional changes in the central nervous system. We now show that the lifelong depletion of the sex hormone E2 in female FORKO mice correlates with abnormal behavior associated with defined alterations in brain morphology early in life, especially in aged animals. Immunohistochemical studies showed significant increases in the size and number of immunoreactive glial fibrillary acidic protein glial cells found in several brain regions (cortex and hippocampus) and a dramatic decline in estrogen receptors alpha and beta in the amygdala of FORKO females. These changes were associated with increased signs of anxiety in these animals. In the present study, we provide evidence that the chronic depletion of sex hormone E2 from early development leads to neural impairments in adult and aged FORKO mice that are associated with hypertrophy of glial cells, cell loss in distinct brain regions, and abnormal behavior. We suggest that the hormonal imbalance found in the female FORKO mouse provides an experimental paradigm for the study of morphological correlates of the behavioral changes that often accompany menopause in women.     

Development of galanin-like immunoreactivity in the brain of the brown trout (Salmo trutta fario), with some observations on sexual dimorphism

The development of galanin-like immunoreactive (GAL-ir) cells and fibers was investigated in the brain of brown trout embryos, alevins, juveniles, and adults (some spontaneously releasing their gametes). The earliest GAL-ir neurons appeared in the preoptic region and the primordial hypothalamic lobe of 12-mm embryos. After hatching, new GAL-ir neurons appeared in the lateral, anterior, and posterior tuberal nuclei, and in late alevins, GAL-ir neurons appeared in the area postrema. In juveniles, further GAL-ir populations appeared in the nucleus subglomerulosus and magnocellular preoptic nucleus. The GAL-ir neuronal groups present in juveniles were also observed in sexually mature adults, although the area postrema of males lacked immunoreactive neurons. Moreover, spawning males exhibited GAL-ir somata in the olfactory bulb and habenula, which were never observed in adult females or in developing stages. In adults, numerous GAL-ir fibers were observed in the ventral telencephalon, preoptic area, hypothalamus, neurohypophysis, mesencephalic tegmentum, ventral rhombencephalon, and area postrema. Moderate to low GAL-ir innervation was seen in the olfactory bulbs, dorsomedial telencephalon, epithalamus, medial thalamus, optic tectum, cerebellum, and rhombencephalic alar plate. There were large differences among regions in the GAL-ir innervation establishment time. In embryos, GAL-ir fibers appeared in the preoptic area and hypothalamus, indicating early expression of galanin in hypophysiotrophic centers. The presence of galanin immunoreactivity in the olfactory, reproductive, visual, and sensory-motor centers of the brain suggest that galanin is involved in many other brain functions. Furthermore, the distribution of GAL-ir elements observed throughout trout development indicates that galaninergic system maturation continues until sexual maturity.     

The health gap in Mexico,measured through child mortality

OBJECTIVE: To estimate the health gap in Mexico, as evidenced by the difference between the observed 1998 mortality rate and the estimated rate and the estimated rate for the same year according to social and economic indicators, with rates from other countries. MATERIAL AND METHODS: An econometric model was developed, using the 1998 child mortality rate (CMR) as the dependent variable, and macro-social and economic indicators as independent variables. The model included 70 countries for which complete data were available. RESULTS: The proposed model explained over 90% of the variability in CMR among countries. The expected CMR for Mexico was 22% lower that the observed rate, which represented nearly 20,000 excess deaths. CONCLUSIONS: After adjusting for differences in productivity, distribution of wealth, and investment in human capital, the excess child mortality rate suggested efficiency problems in the Mexican health system, at least in relation to services intended to reduce child mortality. The English version of this paper is available at: http://www.insp.mx/salud/index.html.