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

Abstract

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 (

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

“…Severe iodine deficiency before and throughout gestation results in a rat model of neurological cretinism (330) with brain alterations similar to those described in human affected populations (342)(343)(344). Given that feeding on LID can potentially decrease fertility, particularly if the state of iodine deficiency is severe enough to reduce serum T 3 , LID alone might not act quickly enough to create a state of iodine deficiency in the fetus.…”

Modulation of adult hippocampal neurogenesis by thyroid hormones: implications in depressive-like behavior

“…Thyroidectomized rats, both untreated and treated, were fed a low iodine diet starting the day of surgery. 21 At the time of killing, both P95 and P120 thyroidectomized rats had greatly decreased T4 and T3 in serum and liver (serum T4 < 1.1 ng/ml and T3 < 0.08 ng/ml; liver T4 < 2.1 ng/g and T3 < 0.70 ng/g), a significant reduction in body weight (BW; P < 0.001), and a 66% reduction of liver type 1 deiodinase (D1) mRNA expression 32 with respect to sham-operated controls. TH treatment consisted in the administration of a physiological combination of T4 and T3 in the drinking water (0.18 mg T4/ml and 0.03 mg T3/ml).…”

“…19 In particular, in the hippocampus, TH deficiency causes reduced growth, reduced number of cells in the DG, and abnormal neuronal migration and maturation. [20][21][22] TH action is mediated through T3 nuclear receptors, and T3 receptor deficiency or mutations also alter adult hippocampal structure and hippocampus-dependent behavior. 23,24 Very recently, TH have been implicated in adult neurogenesis, [25][26][27][28] but little is known on the functional consequences of TH actions on proliferation of neuronal progenitors.…”

The changes of processes of free radical oxidation of lipids and proteins, antioxidant defence in rats with hypofunction of the thyroid gland in conditions of iodine and copper deficiency

“…Дослідження проводили на 60 нелінійних статевозрілих щурах-самцях масою 120-180 г, яких протягом експерименту утримували на йододефіцитній дієті [15]. Усім тваринам моделювали ГЩЗ додаванням до питної води тиреостатичного препарату мерказолілу (7,5 мг/100 г маси тіла) впродовж 14 днів [16].…”

“…Після цього тварини були розділені на дві дослідні групи. Щурів 1-ї групи продовжували утримувати на йододефіцитній дієті (ГЩЗ І , n=30) [15]. Щурам 2-ї групи моделювали дефіцит міді за умов їх пере-бування на йододефіцитній дієті (ГЩЗ І+Cu , n=30).…”