Growth restriction induced by chronic prenatal hypoxia affects breathing rhythm and its pontine catecholaminergic modulation
نویسندگان
چکیده
منابع مشابه
Prematurity and Prenatal Growth Restriction Differently Affects Brain Connectivity
Survival of children born prematurely or with very low birth weight has increased dramatically in the last decades, but the long term developmental outcome remains a concern. The most common cerebral neuro-pathology observed in case of premature birth is a diffuse white matter abnormality. However, many of the children born prematurely present indeed deficits in their cognitive capacities, in p...
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Mammalian target of rapamycin (mTOR) is a protein that regulates cell growth in response to altered nutrient and growth factor availability. Our objective was to assess activated mTOR and its intracellular intermediates p70, and 4EBP1 in placental and invasive trophoblast cells in a hypoxia-induced model of intrauterine growth restriction (IUGR) in rats. Rats were treated with hypoxia (9%) for ...
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The BIO 14.6 hamster (dystrophic), animal model of limb girdle muscular dystrophy, exhibits low plasma triiodothyronine levels, muscle weakness, and decreased breathing. After exposure to acute intermittent bouts of hypoxia, dystrophic hamsters depress ventilation relative to baseline resulting in ventilatory long-term depression (LTD). Control hamsters may increase ventilation relative to base...
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Postnatal rapid growth by excess intake of nutrients has been associated with an increased susceptibility to diseases in neonates with intra-uterine growth restricted (IUGR). The aim of the present study was to determine whether postnatal nutritional restriction could improve intestinal development and immune function of neonates with IUGR using piglets as model. A total of twelve pairs of norm...
متن کاملModulation of chronic hypoxia-induced chemoreceptor hypersensitivity by NADPH oxidase subunits in rat carotid body.
Previous studies in our laboratory established that reactive oxygen species (ROS) generated by NADPH oxidase (NOX) facilitate the open state of a subset of K+ channels in oxygen-sensitive type I cells of the carotid body. Thus pharmacological inhibition of NOX or deletion of a NOX gene resulted in enhanced chemoreceptor sensitivity to hypoxia. The present study tests the hypothesis that chronic...
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ژورنال
عنوان ژورنال: Journal of Neurophysiology
سال: 2016
ISSN: 0022-3077,1522-1598
DOI: 10.1152/jn.00869.2015