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Maternal hypothyroxinemia disrupts neurotransmitter metabolic enzymes in developing brain.
TLDR
The prenatal disturbances noted in this study may have wide-ranging consequences since they occur when neurotransmitters have putative neurotropic roles in brain development and may affect neurotransmission, thereby contributing to the behavioural dysfunction seen in adult progeny of hypothyroxinemic dams.
Thyroid hormone receptor expression in rat placenta.
TLDR
Rat placenta expresses significant levels of c- erbAalpha and -beta transcripts and protein, providing a possible mechanism of action for T(3) of maternal and fetal origin in this tissue.
Influence of maternal hyperthyroidism in the rat on the expression of neuronal and astrocytic cytoskeletal proteins in fetal brain.
TLDR
Maternal hyperthyroidism compromises the expression of neuronal cytoskeletal proteins in late fetal brain, suggestive of a pattern of accelerated neuronal differentiation.
Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta.
TLDR
Maternal hypothyroxinemia results in fetal growth retardation and impaired brain development before the onset of fetal thyroid function, and these deficits are present during the critical period of neuroblast proliferation and may contribute to long term changes in brain development and function seen in this model and in the progeny of Hypothyroxinemic women.
Maternal thyroid status regulates the expression of neuronal and astrocytic cytoskeletal proteins in the fetal brain.
TLDR
It is confirmed that maternal hypothyroidism disrupts early fetal brain development and early disturbances in neuronal differentiation are not corrected by the onset of fetal TH secretion, contributing to the neurological damage observed in children born to hypothyroxinaemic mothers.
Maternal hypothyroidism in the rat influences placental and liver glycogen stores: fetal growth retardation near term is unrelated to maternal and placental glucose metabolic compromise.
TLDR
Multiple regression analyses indicate that these fetal deficits are strongly associated with the retardation in fetal growth, while the elevated maternal liver and placental glycogen concentrations have no impact on fetal growth near term.
SHORT COMMUNICATION maternal thyroid dysfunction and c- fos and c- jun expression in rat placenta.
TLDR
Maternal hypothyroidism may induce c- fos/c- jun -related placental dysfunction, but only relatively late in gestation when fetal thyroid function is already established.
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