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, we have used the chicken embryo to study the effect of maternal MMI treatment on the developing embryo. It has been shown earlier that MMI is taken up from the egg by the embryo and is capable of disturbing development, including brain development
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Introduction The actions of thyroid hormones (TH) on brain development and function are among the more relevant of these hormones, strongly influencing neuromotor performance, cognition and mood. Multiple conditions cause impaired TH action
Department of Endocrinology and Metabolism, The Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China Medical University, Department of Geriatrics, Shenyang Northern Hospital, No.155 Nanjing Bei Street, Hepig District, Shenyang 110001, People's Republic of China
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Introduction It is well known that iodine is a trace element essential for the synthesis of triiodothyronine (T 3 ) and thyroxine (T 4 ), which play a crucial role in the process of early growth and development of most organs, especially the brain
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( 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
Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
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Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
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Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
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Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada
Graduate Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, Canada
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tissues such as the brain ( Sapolsky et al. 2000 ). Interestingly, the effects of ELS on brain development are often studied using stressors given within the SHRP (e.g. PND5 in mice) when blood GC levels are extremely low. Common models of ELS include
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Introduction Thyroid hormones are crucial for brain development, acting through nuclear receptors for T3 to control gene expression ( Brent 2012 , Mendoza & Hollenberg 2017 ). The amount of T3 reaching the nucleus of target cells depends
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ABSTRACT
Tri-iodothyronine (T3) binding studies were performed on neuronal and glial nuclei prepared from developing rats brain by discontinuous sucrose gradient centrifugation. Maximum binding capacities (MBC) and dissociation constants (K d) were obtained from Eadie-Hofstee plots of transformed data. An ontogenic study on nuclei prepared from whole brain revealed that on day 5 after birth, glial nuclear MBC was 1774±201 (s.e.m.) fmol/mg DNA compared with 974±117 fmol/mg DNA for the neurones (P<0·01). Although diminishing to 667±112 fmol/mg DNA by day 21, alterations in neuronal MBC over the neonatal period were not statistically significant, whereas glial MBC diminished steadily to 557±133 fmol/mg DNA in glial nuclei (P<0·05). Over the same period, a significant reduction in K d was noted only in the glia, from 3·17±0·40 to 1·83±0·34 nmol/l (P<0·03). Ligand specificity of the receptor in both nuclear types on day 21 was tri-iodoacetic acid > T3 > thyroxine > 3,3′,5′-T3, but this was less clearly demonstrated at day 5.
Regional studies on days 15 and 21 demonstrated that for both neuronal and glial nuclei, receptors are concentrated in the cerebral cortex and diminish in a cranio-caudal direction. Cerebral glial MBC on day 21 was 2215±147 fmol/mg DNA, at this stage still exceeding the cerebral neuronal capacity of 1111±207fmol/mg DNA. The results indicate that neonatal glia may respond directly to thyroid hormones via nuclear receptor binding, and that receptors are predominantly located in the cortex. Decreases in average MBC in the late neonate may be due to increases in the numbers of cells containing fewer nuclear receptors.
Journal of Endocrinology (1990) 126, 409–415
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SUMMARY
Some developmental and functional manifestations of thyroxine (T4) administered on the first 2 days of postnatal life were studied in the female rat. Brain myelinogenesis estimated by brain esterified cholesterol concentration, and brain myelin age estimated by brain total cholesterol concentration, were subsequently determined. Thyroxine treatment resulted in a greater concentration of esterified cholesterol in the brain than saline treatment, but the latter appeared to delay the normal increase shown by non-injected controls. Thyroxine treatment resulted in total and free cholesterol levels similar to those of non-injected controls, these again being greater than those in saline-treated rats. Cholesterol concentrations in liver and serum were not affected by T4 or saline treatment.
Administration of T4 to female rats before administration of 1·25 mg testosterone propionate on day 7 resulted in an ovarian and uterine weight response to human chorionic gonadotrophin (HCG, 1 i.u./day on days 23–26) on day 27 that was greater than that in litter-mates given saline at birth before testosterone propionate and HCG treatment. Postnatal T4 treatment alone in the female was also associated with a reduced thyroid and pituitary gland enlargement after 7 days of propylthiouracil feeding (0·015% in tap water, days 24–31 of life) when compared with either saline or non-injected controls.
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Department of Biological and Environmental Sciences, Department of Human and Social Sciences, School of Medicine, University of Messina, Torre Biologica, Policlinico Universitario Via C. Valeria, Gazzi, 98100 Messina, Italy
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attenuate the development of acute brain injury 1 and 6 h after TBI. On the contrary, combination therapy with melatonin and DEX reduced the degree of brain injury and inflammatory cell infiltration (D). The image shown is representative of at least three
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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
