Dynamic mRNA distribution pattern of thyroid hormone transporters and deiodinases during early embryonic chicken brain development

Neuroscience ◽  
2012 ◽  
Vol 221 ◽  
pp. 69-85 ◽  
Author(s):  
S. Geysens ◽  
J.L. Ferran ◽  
S.L.J. Van Herck ◽  
P. Tylzanowski ◽  
L. Puelles ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Brain Development ◽  
Distribution Pattern ◽  
Chicken Brain ◽  
Embryonic Chicken

Expression profile and thyroid hormone responsiveness of transporters and deiodinases in early embryonic chicken brain development

2012 ◽  
Vol 349 (2) ◽  
pp. 289-297 ◽  
Author(s):  
Stijn L.J. Van Herck ◽  
Stijn Geysens ◽  
Joke Delbaere ◽  
Przemko Tylzanowski ◽  
Veerle M. Darras
Keyword(s):  
Thyroid Hormone ◽  
Brain Development ◽  
Expression Profile ◽  
Chicken Brain ◽  
Embryonic Chicken ◽  
Hormone Responsiveness

Regulators of thyroid hormone availability and action in embryonic chicken brain development

2013 ◽  
Vol 190 ◽  
pp. 96-104 ◽  
Author(s):  
Stijn L.J. Van Herck ◽  
Stijn Geysens ◽  
Joke Delbaere ◽  
Veerle M. Darras
Keyword(s):  
Thyroid Hormone ◽  
Brain Development ◽  
Chicken Brain ◽  
Embryonic Chicken

scholarly journals Properties of Some Glycosyltransferases in Embryonic Chicken Brain

1970 ◽  
Vol 245 (24) ◽  
pp. 6607-6615 ◽  
Author(s):  
Halina Den ◽  
Bernard Kaufman ◽  
Saul Roseman
Keyword(s):  
Chicken Brain ◽  
Embryonic Chicken

scholarly journals Evidence for Prenatal Exposure to Thyroid Disruptors and Adverse Effects on Brain Development

2019 ◽  
Vol 8 (6) ◽  
pp. 283-292 ◽  
Author(s):  
Barbara A. Demeneix
Keyword(s):  
Thyroid Hormone ◽  
Brain Development ◽  
Prenatal Exposure ◽  
Thyroid Hormone Receptor ◽  
Placental Transfer ◽  
Chemical Exposure ◽  
Autism Spectrum ◽  
Consumer Products ◽  
Neurodevelopmental Disease ◽  
Neuronal Stem Cell

Thyroid hormone regulates vital processes in early brain development such as neuronal stem cell proliferation, migration, and myelination. The fetal thyroid is not fully functional until mid-pregnancy (18–20 weeks), so placental transfer of maternal thyroid hormones during early pregnancy is crucial, as is the maternal iodine status. The volume of chemical production has increased 300-fold since the 1970s. Thus, chemical exposure is ubiquitous; every child born today has dozens of man-made xenobiotic compounds in its blood. Increasing evidence from both epidemiological and animal or in vitro studies demonstrates that many of these chemicals have the potential to interfere with thyroid hormone availability and action at different physiological levels. These chemicals are found in numerous consumer products and include certain plastics, pesticides, perfluorinated compounds, and flame retardants. The last decades have seen exponential increases in neurodevelopmental disease including autism spectrum disorder and attention deficit/hyperactivity disorder. We hypothesize that prenatal exposure to mixtures of thyroid hormone-disrupting chemicals, with iodine deficiency potentially exacerbating the situation, has a strong probability of contributing to this increased incidence of neurodevelopmental disease, but could also entail a surreptitious, but socio-economically consequential, loss of IQ. Thyroid hormone receptor actions can modulate gene transcription, most often through epigenetic mechanisms. Thus, interference with epigenetic regulations is increasingly thought to link neurodevelopmental disease and IQ loss to thyroid hormone disruption.

scholarly journals Thyroid Hormone Insufficiency during Brain Development Reduces Parvalbumin Immunoreactivity and Inhibitory Function in the Hippocampus

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 92-102 ◽  
Author(s):  
M. E. Gilbert ◽  
L. Sui ◽  
M. J. Walker ◽  
W. Anderson ◽  
S. Thomas ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Brain Development ◽  
Dentate Gyrus ◽  
Perforant Path ◽  
High Dose ◽  
Synaptic Inhibition ◽  
Inhibitory Function ◽  
Inhibitory Circuitry ◽  
Dose Dependent

Thyroid hormones are necessary for brain development. γ-Amino-butyric acid (GABA)ergic interneurons comprise the bulk of local inhibitory circuitry in brain, many of which contain the calcium binding protein, parvalbumin (PV). A previous report indicated that severe postnatal hypothyroidism reduces PV immunoreactivity (IR) in rat neocortex. We examined PV-IR and GABA-mediated synaptic inhibition in the hippocampus of rats deprived of thyroid hormone from gestational d 6 until weaning on postnatal d 30. Pregnant dams were exposed to propylthiouracil (0, 3, 10 ppm) via the drinking water, which decreased maternal serum T4 by approximately 50–75% and increased TSH. At weaning, T4 was reduced by approximately 70% in offspring in the low-dose group and fell below detectable levels in high-dose animals. PV-IR was diminished in the hippocampus and neocortex of offspring killed on postnatal d 21, an effect that could be reversed by postnatal administration of T4. Dose-dependent decreases in the density of PV-IR neurons were observed in neocortex and hippocampus, with the dentate gyrus showing the most severe reductions (50–75% below control counts). Altered staining persisted to adulthood despite the return of thyroid hormones to control levels. Developmental cross-fostering and adult-onset deprivation studies revealed that early postnatal hormone insufficiency was required for an alteration in PV-IR. Synaptic inhibition of the perforant path-dentate gyrus synapse evaluated in adult offspring, in vivo, revealed dose-dependent reductions in paired pulse depression indicative of a suppression of GABA-mediated inhibition. These data demonstrate that moderate degrees of thyroid hormone insufficiency during the early postnatal period permanently alters interneuron expression of PV and compromises inhibitory function in the hippocampus.

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