Ontogenesis of Hypothalamic-Pituitary-Thyroid Function and Metabolism in Man, Sheep, and Rat

Fisher, Delbert A.; Dussault, Jean H.; Sack, Joseph; Chopra, Inder J.

doi:10.1016/b978-0-12-571133-3.50010-6

Cited by 246 publications

(240 citation statements)

References 73 publications

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“…The effectiveness of the treatment was further confirmed by RIA assessement in serum of T4, the major circulating thyroid hormone. As expected from thyroid function in the developing rats (Fisher et al, 1977), T4 levels rose sharply in normal animals during the first 2 postnatal weeks of life. At birth, the T4 concentration in serum averaged 0.9 ng/ml and reached 18.8 and 52.4 ng/ml (means from two animals) at P7 and P14, respectively.…”

Section: Microglial Development In Hypothyroid Ratsmentioning

confidence: 67%

“…The early postnatal stages, however, appeared to be critical for thyroid hormone-stimulated accumulation of microglial cells. The density of microglial cells in the cingulate cortex of hypothyroid rats dropped below normal levels between P0 and P4, whereas injection of T3 during this period of development increased microglial density above normal levels, suggesting that during this developmental period the low endogenous production of thyroid hormone (Fisher et al, 1977) could limit the growth of cortical microglia. In contrast, between P4 and P7, cortical microglia expanded in both normal and hyperthyroid rats, but also in hypothyroid animals.…”

Section: Thyroid Hormone Favors Microglia Expansion: Early Postnatal mentioning

confidence: 99%

“…Thyroid hormone in fetal rats is supplied by the mother and, from E17, by the fetal thyroid (Fisher et al, 1977;Kawaio and Tsuneda, 1985). In our study, hypothyroid rats were obtained by continuous administration, from E16, of an anti-thyroid drug (MTU) that inhibited both maternal and fetal thyroid glands.…”

Section: Thyroid Hormone Favors Microglia Expansion: Early Postnatal mentioning

confidence: 99%

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Regulation of Microglial Development: A Novel Role for Thyroid Hormone

et al. 2001

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The postnatal development of rat microglia is marked by an important increase in the number of microglial cells and the growth of their ramified processes. We studied the role of thyroid hormone in microglial development. The distribution and morphology of microglial cells stained with isolectin B4 or monoclonal antibody ED1 were analyzed in cortical and subcortical forebrain regions of developing rats rendered hypothyroid by prenatal and postnatal treatment with methyl-thiouracil. Microglial processes were markedly less abundant in hypothyroid pups than in age-matched normal animals, from postnatal day 4 up to the end of the third postnatal week of life. A delay in process extension and a decrease in the density of microglial cell bodies, as shown by cell counts in the developing cingulate cortex of normal and hypothyroid animals, were responsible for these differences. Conversely, neonatal rat hyperthyroidism, induced by daily injections of 3,5,3Ј-triiodothyronine (T3), accelerated the extension of microglial processes and increased the density of cortical microglial cell bodies above physiological levels during the first postnatal week of life.Reverse transcription-PCR and immunological analyses indicated that cultured cortical ameboid microglial cells expressed the ␣1 and ␤1 isoforms of nuclear thyroid hormone receptors. Consistent with the trophic and morphogenetic effects of thyroid hormone observed in situ, T3 favored the survival of cultured purified microglial cells and the growth of their processes. These results demonstrate that thyroid hormone promotes the growth and morphological differentiation of microglia during development.

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Section: Microglial Development In Hypothyroid Ratsmentioning

confidence: 67%

Section: Thyroid Hormone Favors Microglia Expansion: Early Postnatal mentioning

confidence: 99%

Section: Thyroid Hormone Favors Microglia Expansion: Early Postnatal mentioning

confidence: 99%

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Regulation of Microglial Development: A Novel Role for Thyroid Hormone

et al. 2001

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“…The function of the mammalian thyroid gland during the perinatal period has received much attention during the past few years (Geloso, 1967 ; Thorburn and Hopkins, 1973 ;Vigouroux, 1976 ;Fisher et al, 1977). However, to our knowledge there are very few sequential studies of the plasma iodothyronine level in newborn calves (Nathanielsz, 1969 ;Kahl, Wrenn and Bitman, 1977 ;Cabello, 1980).…”

mentioning

confidence: 99%

Thyroxine, triiodothyronine and iodide in different breeds of newborn calves

Davicco¹,

Vigouroux²,

Dardillat³

et al. 1982

Reprod. Nutr. Dévelop.

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Summary. Plasma thyroxine (T 4 ), triiodothyronine (T 3 ) and iodide levels were measured from birth until 30 days of age in 17 Holstein x Friesian (HF), 7 Salers and 7 Charolais calves born at term. The response of plasma T 4 and T 3 levels to bovine thyrotropin (TSH) injection was also compared in two groups of 9 HF calves 3hrs and 21 days, respectively, after birth.In the HF calves, plasma T 4 and T 3 levels increased from birth to 6 hrs (when the rectal temperature of these calves decreased slightly), then diminished until day 7 and remained stable until 30 days of age. In Salers calves, changes in the plasma T 4 and T 3 levels were not different from those observed in HF animals. However, in Charolais calves, there was no significant increase in plasma T 4 and T 3 levels after birth. Twelve and 24 hrs after birth, the plasma iodothyronine levels measured in these animals were lower than in HF calves. In Salers and Charolais calves a positive linear relationship was demonstrated between plasma T 4 (or T 3 ) levels at birth and the birth weight. In the three groups of calves, plasma iodide levels decreased from birth until 10 days of age, then remained stable until the end of the first neonatal month.Intravenous injection of the same dose of bovine TSH (5 mU/kg of body weight) induced a rise in the plasma T 4 and T 3 levels which was significantly more intense in 21-day old calves than in 3-hr old calves.Introduction.

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“…Finally, fetal blqod analysis of T 3 and TSH levels following delivery showed no evidence of T 3 reaching the fetal compartment. FISHER et al [10] have demonstrated a suppression of TSH in human neonates 12-24 hours after intraamniotic injection of T 4 . Those cases were not stressed pregnancies with depressed infants.…”

Section: Discussionmentioning

confidence: 99%