Inherited tertiary hypothyroidism in Sprague–Dawley rats

Lungu, Gina; Xie, Xueyi; Abbott, Louise C.; Stoica, Heidi M.; Jaques, John T.

doi:10.1016/j.brainres.2007.02.042

Cited by 14 publications

(12 citation statements)

References 37 publications

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“…Several reports are listed on the harmful effect of thyroid hormone deficiency during the development (Nicholson and Altman, 1972a; Lauder, 1977a,b; Stein et al, 1991; Porterfield and Hendrich, 1993; Bernal and Nunez, 1995; Oppenheimer and Schwartz, 1997; Anderson, 2001; Wong and Leung, 2001; Lavado‐Autric et al, 2003; Lee et al, 2003; Farwell et al, 2005; Koibuchi, 2006; Stoica et al, 2007). Taken together, hypothyroidism can be classified based on its time of onset (congenital or acquired), severity (overt {clinical} or mild {subclinical}), and the degree of endocrine aberration (primary or secondary) (Roberts and Ladenson, 2004).…”

Section: Hypothyroidism and Brain Development Interactionsmentioning

confidence: 99%

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

276

254

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The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.

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Section: Hypothyroidism and Brain Development Interactionsmentioning

confidence: 99%

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

276

254

View full text Add to dashboard Cite

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“…Thyroid hormones (THs) are essential for the proper development of numerous tissues, notably the brain (Carageorgiou et al, 2007; Ahmed et al, 2008; Visser et al, 2008; Zoeller, 2008; Ahmed et al, 2010). Also, several reports are listed on the harmful effect of TH deficiency during the development (Koibuchi, 2006; Carageorgiou et al, 2007; Stoica et al, 2007; Ahmed et al, 2008; Hasebe et al, 2008). A number of other authors (Higuchi et al, 2001; Jaeggi and Roman, 2006; Ahmed et al, 2008, 2010) recorded that hyperthyroidism is accompanied by THs increment during the development.…”

Section: Introductionmentioning

confidence: 99%

Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II—The developmental pattern of neurons in relation to oxidative stress and antioxidant defense system

Ahmed

El-Gareib

et al. 2012

Intl J of Devlp Neuroscience

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Excessive concentrations of free radicals in the developing brain may lead to neurons maldevelopment and neurons damage and death. Thyroid hormones (THs) states play an important role in affecting the modulation of oxidative stress and antioxidant defense system. Thus, the objective of this study was to clarify the effect of hypothyroidism and hyperthyroidism in rat dams on the neurons development of different brain regions of their offspring at several postnatal weeks in relation to changes in the oxidative stress and antioxidant defense system. The adult female rats were administered methimazole (MMI) in drinking water (0.02% w/v) from gestation day 1 to lactation day 21 to induce hypothyroidism and exogenous thyroxine (T4) in drinking water (0.002% w/v) beside intragastric incubation of 50--200 T4 μg/kg body weight (b. wt.) to induce hyperthyroidism. In normal female rats, the sera total thyroxine (TT4) and total triiodothyronine (TT3) levels were detectably increased at day 10 post-partum than those at day 10 of pregnancy. Free thyroxine (FT4), free triiodothyronine (FT3), thyrotropin (TSH) and growth hormone (GH) concentrations in normal offspring were elevated at first, second and third postnatal weeks in an age-dependent manner. In hypothyroid group, a marked depression was observed in sera of dam TT3 and TT4 as well as offspring FT3, FT4 and GH, while there was a significant increase in TSH level with the age progress. The reverse pattern to latter state was recorded in hyperthyroid group. Concomitantly, in control offspring, the rate of neuron development in both cerebellar and cerebral cortex was increased in its density and complexity with age progress. This development may depend, largely, on THs state. Both maternal hypothyroidism and hyperthyroidism caused severe growth retardation in neurons of these regions of their offspring from the first to third weeks. Additionally, in normal offspring, seven antioxidant enzymes, four non-enzymatic antioxidants and one oxidative stress marker (lipid peroxidation, LPO) followed a synchronized course of alterations in cerebrum, cerebellum and medulla oblongata. In both thyroid states, the oxidative damage has been demonstrated by the increased LPO and inhibition of enzymatic and non-enzymatic antioxidants in most examined ages and brain regions. These disturbances in the antioxidant defense system led to deterioration in the neuronal maturation and development. In conclusion, it can be suggested that the maldevelopment of neurons and dendrites in different brain regions of offspring of hypothyroid and hyperthyroid mother rat dams may be attributed, at least in part, to the excess oxidative stress and deteriorated antioxidant defense system in such conditions.

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“…In contrast, induction of hypothyroidism by administration of methimazole in pregnant rats and then continuing administration of methimazole to the weanling offspring decreased both striatial D1 receptor protein levels and D1 stimulation of adenylate cyclase activity. Since induction of hypothyroidism prenatally and during critical periods of development can also have marked effects on brain morphology (Stoica et al, 2007), changes in D1 receptor levels may have been associated with this factor. Thus, both age and duration of hypothyroidism appear to affect D1 expression and function.…”

Section: Introductionmentioning

confidence: 99%

Hypothyroidism attenuates SCH 23390-mediated depression of breathing and decreases d1 receptor expression in carotid bodies, PVN and striatum of hamsters

Schlenker

Schultz

2011

Brain Research

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Hypothyroidism can lead to depressed breathing. We determined if propylthiouracil (PTU)–induced hypothyroidism in hamsters (HH) altered dopamine D1 receptor expression, D1 receptor-modulated ventilation, and ventilatory chemoreflex activation by hypoxia or hypercapnia. Hypothyroidism was induced by administering 0.04% PTU in drinking water for three months. Ventilation was evaluated following saline or 0.25 mg/kg SCH 23390, a D1 receptor antagonist, while awake hamsters breathed normoxic (21% O2 in N2), hypoxic (10% O2 in N2) and hypercapnic (5% CO2 in O2) air. Relative to euthyroid hamsters (EH), HH exhibited decreased D1 receptor protein levels in carotid bodies, striatum, and hypothalamic paraventricular nucleus, but not in the nucleus tractus solitarius. Relative to EH, HH exhibited lower ventilation during exposure to normoxia, hypoxia, or hypercapnia, but comparable ventilatory responsiveness to chemoreflex activation. SCH 23390 decreased ventilation of EH hamsters exposed to normoxia, hypoxia, and hypercapnia. In HH SCH 23390 increased ventilation during baseline normoxia and did not affect ventilation during exposure to hypoxia and hypercapnia, resulting in reduced ventilatory responsivess to chemoreflex activation by hypoxia and hypercapnia. Furthermore, in HH D1 receptor protein levels are decreased in several brain regions and within the carotid bodies. Moreover, D1 receptor-modulation of breathing at rest and during gas exposures were depressed in EH but not HH.

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Inherited tertiary hypothyroidism in Sprague–Dawley rats

Cited by 14 publications

References 37 publications

Thyroid hormones states and brain development interactions

Thyroid hormones states and brain development interactions

Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II—The developmental pattern of neurons in relation to oxidative stress and antioxidant defense system

Hypothyroidism attenuates SCH 23390-mediated depression of breathing and decreases d1 receptor expression in carotid bodies, PVN and striatum of hamsters

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