Severe hypothyroidism and the maturation of the rat cerebral cortex

Ruiz-Marcos, Antonio; Sánchez-Toscano, Fernando; F, Escobar del Rey; G, Morreale de Escobar

doi:10.1016/0006-8993(79)90292-0

Cited by 86 publications

(40 citation statements)

References 21 publications

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“…In adult progeny of rats fed a diet prepared with components from a severely iodine-deficient area of China, Chen et al (42) show that the number of dendritic spines on the shaft of pyramidal neurons of the cerebral cortex was reduced as compared to that of progeny from rats fed the same diet, but supplemented with iodine. However, the parameter they measured is not only sensitive to hypothyroidism of neonatal onset (43), but also to adult onset hypothyroidism (44), and the alterations were not necessarily because of early brain damage. Permanent audiogenic seizure susceptibility was shown in adult progeny of severely iodinedeficient rats (45), but the timing of the initial damage was not defined.…”

Section: Discussionmentioning

confidence: 99%

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Martinez-Galán¹,

Pedraza²,

Santacana³

et al. 1997

J. Clin. Invest.

104

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The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth and related to maternal hypothyroxinemia before mid gestation. However, direct evidence of this etiopathogenic mechanism is lacking. Rats were fed diets with a very low iodine content (LID), or LID supplemented with KI. Other rats were fed the breeding diet with a normal iodine content plus a goitrogen, methimazole (

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Section: Discussionmentioning

confidence: 99%

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Martinez-Galán¹,

Pedraza²,

Santacana³

et al. 1997

J. Clin. Invest.

104

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“…Indeed, a number of studies performed by Ruiz-Marcos and colleagues have characterized a potentially important effect of thyroid status on cortical neurons. These researchers measured the density of dendritic spines of layer V pyramidal neurons in control and thyroidectomized rats and determined that hypothyroidism causes a significant reduction in their number (Kalaria and Prince 1986;Ruiz-Marcos et al 1979, 1980. This effect was present in both juvenile and adult rats and could be reversed, in a dose-dependant fashion, by thyroxine treatment.…”

Section: Do Thyroid Hormones Also Exert Neurotrophic Effects?mentioning

confidence: 99%

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for Difficult-to-Treat depression

Manji

Quiróz

Sporn

et al. 2003

Biological Psychiatry

445

259

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“…Hypothyroidism decreases neural axonal density and growth in the cerebral cortex (71) and reduces the dendrite branching of Purkinje cells in the cerebellum (72), pyramidal cells in the cerebral cortex (73), and cortical neurons of the corpus callosum (74). Rami and Rabie (75) report a delay in hippocampal synaptogenesis under hypothyroid conditions, based on measurements of synaptophysin, a marker protein of mature synaptic vesicles.…”

Section: Thyroid Hormone Influence On Brain Developmentmentioning

confidence: 99%

A model of the development of the brain as a construct of the thyroid system.

Howdeshell

2002

Environ Health Perspect

333

237

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Thyroid hormone is essential for normal brain development. However, little is known about the molecular and cellular mechanisms that mediate thyroid hormone action on the developing brain or the developmental events selectively affected. Consequently, although a large number of environmental chemicals interfere with the thyroid system, there are few neurodevelopmental end points to recruit for toxicological studies. Therefore, my goal here is to review what is known about the relative timing of normal brain construction and thyroid system development, with special focus on the period of in utero development in humans and the comparable developmental period in laboratory rats. These data are presented as a timeline to aid in the identification of thyroid-sensitive end points in brain development and to highlight important data gaps. I discuss the known influence of certain synthetic chemicals on the thyroid system and include a brief review of the effects of developmental exposure to chemicals on thyroid system function. The relationship between the thyroid hormone and retinoic acid systems, as well as the thyroid hormone sensitivity of the developing cochlea, is also discussed.

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Severe hypothyroidism and the maturation of the rat cerebral cortex

Cited by 86 publications

References 21 publications

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for Difficult-to-Treat depression

A model of the development of the brain as a construct of the thyroid system.

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