scholarly journals Comparison of Iodothyronine 5′-Deiodinase and Other Thyroid-Hormone-dependent Enzyme Activities in the Cerebral Cortex of Hypothyroid Neonatal Rat

1982 ◽  
Vol 70 (5) ◽  
pp. 1110-1123 ◽  
Author(s):  
J. Enrique Silva ◽  
P. Reed Larsen
Endocrinology ◽  
2012 ◽  
Vol 153 (11) ◽  
pp. 5668-5680 ◽  
Author(s):  
Thomas W. Bastian ◽  
Jeremy A. Anderson ◽  
Stephanie J. Fretham ◽  
Joseph R. Prohaska ◽  
Michael K. Georgieff ◽  
...  

Abstract Copper (Cu), iron (Fe), and thyroid hormone (TH) deficiencies produce similar defects in late brain development including hypomyelination of axons and impaired synapse formation and function, suggesting that these micronutrient deficiencies share a common mechanism contributing to these derangements. We previously demonstrated that fetal/neonatal Cu and Fe deficiencies lower circulating TH concentrations in neonatal rats. Fe deficiency also reduces whole-brain T3 content, suggesting impaired TH action in the developing Fe-deficient brain. We hypothesized that fetal/neonatal Cu and Fe deficiencies will produce mild or moderate TH deficiencies and will impair TH-responsive gene expression in the neonatal cerebral cortex and hippocampus. To test this hypothesis, we rendered pregnant Sprague Dawley rats Cu-, Fe-, or TH-deficient from early gestation through postnatal d 10 (P10). Mild and moderate TH deficiencies were induced by 1 and 3 ppm propylthiouracil treatment, respectively. Cu deficiency did not significantly alter serum or tissue TH concentrations or TH-responsive brain mRNA expression. Fe deficiency significantly lowered P10 serum total T3 (45%), serum total T4 (52%), whole brain T3 (14%), and hippocampal T3 (18%) concentrations, producing a mild TH deficiency similar to 1 ppm propylthiouracil treatment. Fe deficiency lowered Pvalb, Enpp6, and Mbp mRNA levels in the P10 hippocampus. Fe deficiency also altered Hairless, Dbm, and Dio2 mRNA levels in the P10 cerebral cortex. These results suggest that some of the brain defects associated with Fe deficiency may be mediated through altered thyroidal status and the concomitant alterations in TH-responsive gene transcription.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Fabrice Chatonnet ◽  
Frédéric Picou ◽  
Teddy Fauquier ◽  
Frédéric Flamant

Thyroid hormones (TH, including the prohormone thyroxine (T4) and its active deiodinated derivative 3,,5-triiodo-L-thyronine (T3)) are important regulators of vertebrates neurodevelopment. Specific transporters and deiodinases are required to ensure T3 access to the developing brain. T3 activates a number of differentiation processes in neuronal and glial cell types by binding to nuclear receptors, acting directly on transcription. Only few T3 target genes are currently known. Deeper investigations are urgently needed, considering that some chemicals present in food are believed to interfere with T3 signaling with putative neurotoxic consequences.


2011 ◽  
pp. P1-662-P1-662
Author(s):  
Thomas W Bastian ◽  
Jeremy Anderson ◽  
Stephanie J Fretham ◽  
Joseph R Prohaska ◽  
Michael K Georgieff ◽  
...  

Neuroscience ◽  
2002 ◽  
Vol 110 (1) ◽  
pp. 19-28 ◽  
Author(s):  
H Vara ◽  
B Martı́nez ◽  
A Santos ◽  
A Colino

Metabolism ◽  
1990 ◽  
Vol 39 (10) ◽  
pp. 1049-1055 ◽  
Author(s):  
Takashi Nomura ◽  
Marietta Borges ◽  
Sidney H. Ingbar ◽  
J.Enrique Silva

Stroke ◽  
1999 ◽  
Vol 30 (9) ◽  
pp. 1916-1924 ◽  
Author(s):  
N. Benjelloun ◽  
S. Renolleau ◽  
A. Represa ◽  
Y. Ben-Ari ◽  
C. Charriaut-Marlangue

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