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Yuhui Liu, Le Zhang, Jing Li, Zhongyan Shan and Weiping Teng

hormone deficiency in female rats with marginal iodine deficiency has a negative impact on BDNF and can further influence the brain development of offspring. Egr1 belongs to the early growth reactive protein family and is also referred to as krox24 or Zif

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Praveen Kumar, Vishwa Mohan, Rohit Anthony Sinha, Megha Chagtoo and Madan M Godbole

unliganded TRs, we hypothesized that inhibiting HDAC activity would block the negative regulation of target genes by unliganded TRs and may restore normal brain development under hypothyroidism. Using rat model of perinatal hypothyroidism, we here demonstrate

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Meredith A Kelleher, Hannah K Palliser, David W Walker and Jonathan J Hirst

( Lackman et al . 2001 ). Placental insufficiency and IUGR have many implications for foetal brain development. Along with clinical observations, animal studies have also revealed the morphological changes and neurological impairments associated with foetal

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Huali Yu, Ye Guo, Yang Zhao, Feng Zhou, Kehan Zhao, Mayuqing Li, Junxiong Wen, Zixuan He, Xiaojuan Zhu and Xiaoxiao He

brain development and function. For instance, maternal stress-triggered GC elevation changes the fetal brain structure, leading to attention and learning deficits in adulthood ( Weinstock 2008 ). Prenatal stress is highly associated with increased

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Ángel Enrique Céspedes Rubio, Maria José Pérez-Alvarez, Catalina Lapuente Chala and Francisco Wandosell

. 2001 ). Estradiol has an important impact on brain development and normal physiology, but also after injury. Cellular targets of its action are both neurons and the main glial cell types (astrocytes, microglia, radial glia and oligodendrocytes

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S Van der Geyten and V M Darras

beyond postnatal day 12 results in abnormal adult pyramidal cells ( Anderson et al. 2003 ). These observations indicated that not only thus does there exist a narrow window in time during which brain development is thyroid hormone sensitive ( Bernal

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Han Yan, Matthew Mitschelen, Georgina V Bixler, Robert M Brucklacher, Julie A Farley, Song Han, Willard M Freeman and William E Sonntag

IGF1 deficiency and replacement on brain gene expression that we expect contribute to long-term modifications in brain development, function, learning and memory. To this end, we used a unique model of GH/IGF1 deficiency (the Lewis dwarf ( dw/dw ) rat

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A J Conley, R M Bernstein and A D Nguyen

. 2009 ), it has been proposed that the evolution of adrenarche extended the maturation of the human brain ( Campbell 2011 ). If this is true, then correlations between the onset (adrenarche) of adrenal androgen secretion and brain development would be

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Shiao Y Chan, Laura A Hancox, Azucena Martín-Santos, Laurence S Loubière, Merlin N M Walter, Ana-Maria González, Phillip M Cox, Ann Logan, Christopher J McCabe, Jayne A Franklyn and Mark D Kilby

8 (MCT8) gene . American Journal of Human Genetics 77 41 – 53 . ( doi:10.1086/431313 ) Tolsa CB Zimine S Warfield SK Freschi M Sancho RA Lazeyras F Hanquinet S Pfizenmaier M Huppi PS 2004 Early alteration of structural and functional brain

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D Sampson, MR Pickard, AK Sinha, IM Evans, AJ Leonard and RP Ekins

Maternal thyroid hormone (TH) crosses the placenta and is postulated to regulate fetal brain development. However, TH-dependent stages of fetal brain development remain to be characterised. We have therefore compared the levels of several neuronal and glial cytoskeletal proteins in fetal brains from normal (N) and partially thyroidectomised (TX) rat dams by immunoblotting. Pregnancies were studied both before and after the onset of fetal TH secretion, which occurs at 17.5 days gestation (dg) in the rat. Maternal hypothyroidism disrupted fetal growth, so that fetal body and brain weights were reduced near term. Vimentin expression was unaffected, however, indicating normal acquisition of neuronal and glial precursor cells. Fetal brain levels of glial fibrillary acidic protein (GFAP) were reduced at 21 dg, suggesting delayed astrocytic differentiation, although regression analysis demonstrated appropriate GFAP levels for brain weight. Levels of alpha-internexin, the earliest neurofilament protein expressed in fetal brain were reduced at 16 dg in TX dams, but increased at 21 dg. The ontogeny of neurofilament-L was also perturbed in these pregnancies, with deficient levels apparent at both 16 and 21 dg. These effects on neuronal cytoskeletal proteins were unrelated to fetal brain growth retardation. These findings confirm that maternal hypothyroidism disrupts early fetal brain development. Early disturbances in neuronal differentiation are not corrected by the onset of fetal TH secretion. Such disturbances may contribute to the neurological damage observed in children born to hypothyroxinaemic mothers.