Severity and timing of early thyroid deficiency as factors in the induction of learning disorders in rats

Davenport, John W.; Gonzalez, Louis M.; Hennies, Richard S.; Hagquist, William W.

doi:10.1016/0018-506x(76)90044-1

Cited by 33 publications

(14 citation statements)

References 8 publications

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“…The ensuing condition known as cretinism in man has its counterpart in other mammals. Indeed, lasting behavioural and biochemical changes occur in rats deprived of thyroid hormone during antenatal or early neonatal life (Eayrs, 1960(Eayrs, , 1961Davenport et al, 1976). Continual thyroid hormone deprivation almost completely arrests linear growth.…”

Section: Introductionmentioning

confidence: 99%

The Action of Thyroid Hormone

Bernal

Refetoff

1977

Clinical Endocrinology

104

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SUMMARYThyroid hormone affects both developmental and metabolic processes. It has a relatively specific effect on the synthesis of a number of enzymes and other proteins. The fundamental cellular mechanism of action seems to be at the level of genetic regulation. It involves interaction with nuclear receptors, leading to an activation of the protein synthesizing machinery. How binding to receptors is coupled to genetic activation is completely unknown. At least part of the metabolic effects of thyroid hormone could be mediated through an interaction with mitochondria and cell membrane, and with some enzymatic systems such as adenylcyclase.

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Section: Introductionmentioning

confidence: 99%

The Action of Thyroid Hormone

Bernal

Refetoff

1977

Clinical Endocrinology

104

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“…In the mouse and rat, autonomous fetal thyroid hormone secretion rises after 16-17 days postconception followed by early neonatal in creases in T4 and subsequently T3. These increases in T4 have been shown to be temporally correlated with somatic development, brain differentiation, and behavioral deve lopment in the rat [11].The hypothyroid neonatal rat demonstrated somatic [8,16,17,29], neuroanatomical [11,12], electrophysiological [11,14] and behavioral abnormalities [7,9,10,14,17,19,22,24,27] [7,10,14,24] and hyperactivity [7,9,27] have been observed. Abnormalities in adaptive learned behavior [7,10,14,17,27] have been seen in more mature rats following neonatal or fetal hypothyroidism.…”

mentioning

confidence: 99%

“…Abnormalities in adaptive learned behavior [7,10,14,17,27] have been seen in more mature rats following neonatal or fetal hypothyroidism. The hypo thyroid rats have also shown delayed vestibular system de velopment [ 12] and delayed and abnormal cerebellar devel opment and delayed cerebral cortical myelination and diffe rentiation [11,23].However, most of the behavioral and anatomical data has come from postnatal rodent hypothyroidism, resulting from surgically produced [ 17] or pharmacologically induced [7,9,10,22,27] hypothyroidism. The pharmacological agents employed to produce both fetal and neonatal hypo thyroidism such as propylthiouracil (PTU) [9,10,22,27] and methimazole [7] may have independent effects as well as causing both maternal and fetal hypothyroidism when given in utero [II].…”

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confidence: 99%

Evaluation and Characterization of the Hypothyroid <i>hyt/hyt </i>Mouse I: Somatic and Behavioral Studies

et al. 1989

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Mice homozygous for the autosomal-recessive gene hypothyroid (hyt) had congenital hypothyroidism of fetal onset after 15 days postconception. Neonatal hyt/hyt mice had reduced serum thyroxine ranging from 1/5 to 1/6 of normal as well as significantly delayed somatic and behavioral development. Delayed somatic development included retarded eye opening and ear raising, and reduced body length and body weight. The hyt/hyt animals compared to their normal littermates demonstrated delayed reflexive behavior and abnormal motor and adaptive behavior. The somatic and behavioral measures clearly distinguished hyt/hyt animals from their normal littermates even without T4 determination. The somatic and reflexive behavioral abnormalities in the hyt/hyt mouse were similar to other rodent models of human congenital hypothyroidism. The hyt/hyt mouse provided an ideal model for exploring the effect of severe primary inherited hypothyroidism related to deficient autonomous fetal thyroid function and was consistent with the hypothesis that thyroid hormone deficit in utero and in the early neonatal period significantly altered functional development.

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“…Thyroid hormone plays a very important role in brain development (Porterfield and Hendrich, 1993), especially during the early postnatal period (Davenport et al, 1976). The presence of adequate circulation of T 4 c o n c e n t r a t i o n is especially critical for normal brain development, because T 3 does not cross the blood brain barrier (Ruiz et al, 1988;Calvo et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Effect of organosulfur compounds on the expression of UDP-glucuronosyltransferase and thyroid hormone level in TCDD-treated rats

Hong

Kim²

1997

Exp Mol Med

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In this study, we investigated the effect of organosulfur compounds including, diallyl sulfide (DAS), garlic extract, and dially disulfide (DADS) on inducible expression of UDP-glucuronosyltransferase (UGT1) and thyroid hormone level in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats. We measured UGT1 gene expression in rat liver and lung tissues after treatments. We found that a correlation was found to exist between UGT1 gene expression and active T 4 concentrations. The total concentration of plasma T 4 decreased in TCDD-alone treated male and female rats compared to control animals (TCDDalone < control). Plasma T 4 concentration in TCDD + DAS, TCDD + garlic extract and TCDD + DADS treated groups were moderately higher than in TCDD alone animals, but lower than control animals. TCDD + DAS, TCDD + garlic extract and TCDD + DADS moderately increased T 4 glucuronidation and moderately reduced total T 4 . The nonthyroidal nature of thyroid hormone reduction observed in this study extends the evidence for microsomal enzyme inducers as indirect thyroid tumor promoters in rats. Furthermore, the results of present study suggest protective effects of DAS, garlic extract, or DADS on TCDDinduced changes.

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Severity and timing of early thyroid deficiency as factors in the induction of learning disorders in rats

Cited by 33 publications

References 8 publications

The Action of Thyroid Hormone

The Action of Thyroid Hormone

Evaluation and Characterization of the Hypothyroid <i>hyt/hyt </i>Mouse I: Somatic and Behavioral Studies

Effect of organosulfur compounds on the expression of UDP-glucuronosyltransferase and thyroid hormone level in TCDD-treated rats

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