Thyroid hormones during the perinatal period are necessary to respiratory network development of newborn rats

2021 ◽  
pp. 113813
Author(s):  
Jean-Philippe Rousseau ◽  
Luana Tenorio-Lopes ◽  
Sergio Cortez Ghio ◽  
Pascale Desjardins ◽  
Stéphanie Fournier ◽  
...  
1998 ◽  
Vol 275 (6) ◽  
pp. R1812-R1821 ◽  
Author(s):  
Isabelle Dumont ◽  
Krishna G. Peri ◽  
Pierre Hardy ◽  
Xin Hou ◽  
Ana Katherine Martinez-Bermudez ◽  
...  

We tested the hypothesis that high prostaglandin levels during the perinatal period might regulate brain nitric oxide synthase (nNOS) expression. nNOS and cyclooxygenase (COX)-2 mRNAs were higher in brain cortex and the periventricular area of newborn rats and pigs compared with adult brain. Nitric oxide synthase activity was also 2.5- to 4-fold higher in newborn than in adult brain. Administration of nonselective COX inhibitor ibuprofen or COX-2 inhibitor nimesulide every 8 h for 24 h to newborn rats and pigs reduced prostaglandin levels and caused comparable reductions in nNOS mRNA, protein, and activity to levels of adults; COX inhibitor-induced changes were prevented by cotreatment with PGE2 analog, 16,16-dimethyl-PGE2, and agonist for the EP3 receptor of PGE2, sulprostone, but not by PGI2 analog carbaprostacyclin, PGD2, EP1 receptor agonist 17-phenyl trinor-PGE2, and EP2 agonist butaprost. Concordant observations were made in vitro and revealed that nNOS expression (detected by NADPH diaphorase reactivity) mostly present in neurons of the deeper cortical layers was reduced by COX inhibitor, and this effect was prevented by EP3agonist. In conclusion, high levels of PGE2 in neonatal brain contribute to the increased expression of nNOS by acting on EP3 receptors; this positive interaction between PGE2 and nNOS might be required physiologically for normal brain development.


1956 ◽  
Vol 93 (1) ◽  
pp. 19-22 ◽  
Author(s):  
J. M. Reiss ◽  
M. Reiss ◽  
A. Wyatt

1986 ◽  
Vol 111 (2) ◽  
pp. 213-216 ◽  
Author(s):  
Ch. Schmid ◽  
Th. Steiner ◽  
E. R. Froesch

Abstract. Osteoblast-like cells prepared from calvaria of newborn rats and grown in culture for 1 week show markedly increased ornithine decarboxylase (ODC) activity upon exposure to parathyroid hormone (PTH) for 4 h. Triiodothyronine (T3) increases ODC activity of the cultures in long-term experiments but does not stimulate cell replication. Moreover, PTH responsiveness is enhanced by T3. Thus, T3 acts directly on bone cells, and the clinical observation of bone sensitization to PTH by thyroid hormones is confirmed at the cellular level.


1989 ◽  
Vol 123 (3) ◽  
pp. 421-428 ◽  
Author(s):  
A. Chatelain ◽  
P. Durand ◽  
E. Naaman ◽  
J. P. Dupouy

ABSTRACT Binding of ACTH to receptors was studied on crude adrenal membranes from fetal and newborn rats. 125I-Labelled ACTH(1–24) was used as the radioligand, the steroidogenic potency of which was 100-fold lower than that of unlabelled ACTH(1–24). Binding was specific, rapidly equilibrated and temperature dependent. Scatchard analysis of the binding data revealed a single class of binding sites with a dissociation constant of about 100 nmol/l at all stages of development studied. The concentration of ACTH receptors expressed per mg membrane proteins decreased in fetuses between days 17 and 21 of gestation and remained stable in newborn rats from weeks 1 to 4. The number of ACTH receptors expressed per adrenal increased regularly in fetal and newborn rats. The perinatal evolution of these concentrations of ACTH receptors is related to the increase in the size of the adrenals and the changes in cytoplasmic structures of the adrenocortical cells. When the number of ACTH-binding sites was expressed per μg DNA, maximum values occurred in fetuses on day 19 of gestation, and minimum values in newborn rats, 1 week after birth. There was an excellent correlation between the plasma levels of immunoreactive ACTH and corticosterone and the number of ACTH receptors per μg DNA during the perinatal period. Other results suggest that ACTH is able to up-regulate the number of its own receptors. Journal of Endocrinology (1989) 123, 421–428


2008 ◽  
Vol 104 (6) ◽  
pp. 1801-1808 ◽  
Author(s):  
Qiuli Liu ◽  
Margaret T. T. Wong-Riley

Previously, we reported a critical period [around postnatal day (P) 12– 13 in the rat] in respiratory network development when distinct neurochemical, metabolic, and physiological changes occur. Since serotonin 2A (5-HT2A) receptors play an important role in respiratory modulation, we hypothesized that they may undergo developmental adjustments during the critical period. Semi-quantitative immunohistochemical analyses were conducted in labeled neurons in a number of brain stem nuclei with or without known respiratory functions from P2 to P21 in rats. Our data indicate that the expressions of 5-HT2A receptors in neurons of the pre-Bötzinger complex, the nucleus ambiguus, and the hypoglossal nucleus were maintained within a relatively narrow range between P2 and P21, with a dip at P3–P4 and a significant reduction only at P12. This change was not observed in the nonrespiratory cuneate nucleus. These results suggest that reduced expressions of 5-HT2A receptors at P12 contributes to neurochemical imbalance within brain stem respiratory nuclei at that time and may be involved in decreased hypoxic ventilatory response at this critical period of development.


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