Long-Term Perspectives of Thyroxine Administration in Neonatal Rats

Varma, Surendra K.; Crawford, John D.

doi:10.1159/000179015

Cited by 11 publications

(7 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The vast majority of cases of excessive serum thyroid hormone concentration seen in pregnancy are due to the overproduction of thyroid hormones (Graves' disease, toxic nodular goiter); in the postpartum period, thyrotoxicosis may be due to exacerbation of Graves' hyperthyroidism or to the release of thyroid hormone due to an acute autoimmune injury to the thyroid tissue (postpartum thyroiditis‐PPT) (Momotani et al, 1994). Furthermore, the neonatal hyperthyroidism leads to permanent decrease in pituitary reserve of TSH secretion (Varma and Crawford, 1979).…”

Section: Thyroid Hormones and Fetal Brain Developmentmentioning

confidence: 99%

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

279

254

View full text Add to dashboard Cite

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.

show abstract

Section: Thyroid Hormones and Fetal Brain Developmentmentioning

confidence: 99%

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

279

254

View full text Add to dashboard Cite

show abstract

“…Thus, it is worth mentioning that maternal THs deficiency may disturb the secretion of other pituitary hormones in their offspring (Wong et al, 1980; Tamasy et al, 1984). Furthermore, neonatal rat's hyperthyroidism (Varma and Crawford, 1979) results in permanent imprinting regarding growth and thyroidal development. Also, Segni and Gorman (2001) speculated that untreated childhood thyrotoxicosis causes accelerated growth.…”

Section: Discussionmentioning

confidence: 99%

“…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. Neonatal hyperthyroidism in rats (Varma and Crawford, 1979) results in permanent decrease in pituitary reserve of thyrotropin (TSH) secretion and permanent imprinting regarding growth and thyroidal development and thus, neonatal period is critical for thyroidal development. Furthermore, hypo‐ or hyperthyroidism affects the maturation of the central nervous system (CNS) and causes irreversible dysfunction of the brain if not corrected shortly after the birth (Wong and Leung, 2001).…”

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

View full text Add to dashboard Cite

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.

show abstract

“…Neonatal hyperthyroidism is associated with hypothyroidism in adulthood [70,71] . Walker and Courtain [72] demonstrated thyroidstimulating hormone (TSH) insensitivity to low T 4 and T 3 concentrations in adult rats treated with T 4 in the neonatal period, in part due to a higher pituitary deiodinase activity.…”

Section: Programming Thyroid Functionmentioning

confidence: 99%

Neonatal Programming of Neuroimmunomodulation – Role of Adipocytokines and Neuropeptides

Moura¹,

Lisboa²,

Passos

2008

Neuroimmunomodulation

101

View full text Add to dashboard Cite

Programming is an epigenetic phenomenon by which nutrition, environment and stress acting in a critical period earlier in life change the organism‘s development. This process was evolutionarily selected as an adaptive tool for the survival of organisms living in nutritionally deficient areas and submitted to stressful conditions. Thus, perinatal malnutrition turns on different genes that provide the organism with a thrifty phenotype. In conditions of abundant supply of nutrients, those programmed organisms can be at risk of developing metabolic diseases (obesity, dyslipidemia, diabetes and hypertension). How nutrition or neonatal stress can program the immune system is less well known. Here, we discuss some of the hormonal and metabolic changes that occur in mothers and neonates and how those factors can imprint hormonal or metabolic changes that program neuroimmunomodulatory effects. Some of these changes involve thyroid hormones, leptin, insulin, glucocorticoids and prolactin as potential imprinting factors. Most of them can be transferred through the milk and may change with malnutrition or stress. We discuss the programming effects of these hormones upon body weight, body composition, insulin action, thyroid, adrenal and immune and inflammatory responses, with special emphasis on leptin, a cytokine that seems to play a central role in these events.

show abstract

Long-Term Perspectives of Thyroxine Administration in Neonatal Rats

Cited by 11 publications

References 10 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

Neonatal Programming of Neuroimmunomodulation – Role of Adipocytokines and Neuropeptides

Contact Info

Product

Resources

About