scholarly journals Thyroid hormone insufficiency alters the expression of psychiatric disorder-related molecules in the hypothyroid mouse brain during the early postnatal period

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Katsuya Uchida ◽  
Kentaro Hasuoka ◽  
Toshimitsu Fuse ◽  
Kenichi Kobayashi ◽  
Takahiro Moriya ◽  
...  

AbstractThe functional role of thyroid hormone (TH) in the cortex and hippocampus of mouse during neuronal development was investigated in this study. TH insufficiency showed a decrease in the expression of parvalbumin (PV) in the cortex and hippocampus of pups at postnatal day (PD) 14, while treatment with thyroxine from PD 0 to PD 14 ameliorated the PV loss. On the other hand, treatment with antithyroid agents in adulthood did not result in a decrease in the expression of PV in these areas. These results indicate the existence of a critical period of TH action during the early postnatal period. A decrease in MeCP2-positive neuronal nuclei was also observed in the cortical layers II–IV of the cerebral cortex. The brains were then stained with CUX1, a marker for cortical layers II–IV. In comparison with normal mice, CUX1 signals were decreased in the somatosensory cortex of the hypothyroid mice, and the total thickness of cortical layers II–IV of the mice was lower than that of normal mice. These results suggest that TH insufficiency during the perinatal period strongly and broadly affects neuronal development.

1991 ◽  
Vol 260 (5) ◽  
pp. H1449-H1454 ◽  
Author(s):  
S. J. Allen ◽  
E. Gunnar Sedin ◽  
A. Jonzon ◽  
A. F. Wells ◽  
T. C. Laurent

Hyaluronan, an important constituent of developmental interstitium in fetal lungs, mediates cell-to-cell interactions and thereby directs migrating cells. Furthermore, because of the polyionic nature of the molecule, hyaluronan forms open, hydrated matrices that provide channels for migrating cells. This hydrated matrix undergoes contraction before birth. However, continued growth of the lung in the perinatal period requires newly synthesized hyaluronan. This study's purpose was to elucidate the changes in lung hyaluronan concentration and distribution in the perinatal period. We studied rabbits at days -6, -4, -2, -1, 0, +2, and +4 with respect to term, as well as adult rabbits. We found that hyaluronan concentration was highest in the youngest fetuses studied [682 +/- 115 micrograms/g dry wt (means +/- SD)]. However, hyaluronan concentration decreased to 129 +/- 12 micrograms/g dry wt just before birth then returned to 366 +/- 111 micrograms/g dry wt at day +4; these values were similar to adult values. We found hyaluronan staining decreased during late gestation, particularly in the interalveolar region. In the postnatal period, hyaluronan staining increased in the visceral pleura and, to a lesser extent, beneath the epithelium of the bronchioles. Hyaluronan did not reaccumulate in the interalveolar region in the postnatal period. Our data suggest a change in the predominant role of lung hyaluronan during the perinatal period. Before term, hyaluronan facilitates morphogenesis. However, hyaluronan's major role in neonatal lung is most likely in regulation of fluid balance in interstitium.


Stress ◽  
2016 ◽  
Vol 19 (4) ◽  
pp. 434-438 ◽  
Author(s):  
Diána Balázsfi ◽  
Lívia Farkas ◽  
Péter Csikota ◽  
Anna Fodor ◽  
Sándor Zsebők ◽  
...  

1997 ◽  
Vol 42 (1) ◽  
pp. 93-102 ◽  
Author(s):  
J P Tan ◽  
F J Seidler ◽  
D A Schwinn ◽  
S O Page ◽  
T A Slotkin

2019 ◽  
Vol 242 (1) ◽  
pp. T145-T160 ◽  
Author(s):  
Natasha N Chattergoon

The fetal heart undergoes its own growth and maturation stages all while supplying blood and nutrients to the growing fetus and its organs. Immature contractile cardiomyocytes proliferate to rapidly increase and establish cardiomyocyte endowment in the perinatal period. Maturational changes in cellular maturation, size and biochemical capabilities occur, and require, a changing hormonal environment as the fetus prepares itself for the transition to extrauterine life. Thyroid hormone has long been known to be important for neuronal development, but also for fetal size and survival. Fetal circulating 3,5,3′-triiodothyronine (T3) levels surge near term in mammals and are responsible for maturation of several organ systems, including the heart. Growth factors like insulin-like growth factor-1 stimulate proliferation of fetal cardiomyocytes, while thyroid hormone has been shown to inhibit proliferation and drive maturation of the cells. Several cell signaling pathways appear to be involved in this complicated and coordinated process. The aim of this review was to discuss the foundational studies of thyroid hormone physiology and the mechanisms responsible for its actions as we speculate on potential fetal programming effects for cardiovascular health.


2021 ◽  
Vol 22 (11) ◽  
pp. 6037
Author(s):  
Dina K. Gaynullina ◽  
Tatiana V. Kudryashova ◽  
Alexander V. Vorotnikov ◽  
Rudolf Schubert ◽  
Olga S. Tarasova

Previously, the abundance of p42/44 and p38 MAPK proteins had been shown to be higher in arteries of 1- to 2-week-old compared to 2- to 3-month-old rats. However, the role of MAPKs in vascular tone regulation in early ontogenesis remains largely unexplored. We tested the hypothesis that the contribution of p42/44 and p38 MAPKs to the contraction of peripheral arteries is higher in the early postnatal period compared to adulthood. Saphenous arteries of 1- to 2-week-old and 2- to 3-month-old rats were studied using wire myography and western blotting. The α1-adrenoceptor agonist methoxamine did not increase the phosphorylation level of p38 MAPK in either 1- to 2-week-old or 2- to 3-month-old rats. Accordingly, inhibition of p38 MAPK did not affect arterial contraction to methoxamine in either age group. Methoxamine increased the phosphorylation level of p42/44 MAPKs in arteries of 2- to 3-month-old and of p44 MAPK in 1- to 2-week-old rats. Inhibition of p42/44 MAPKs reduced methoxamine-induced contractions in arteries of 2- to 3-month-old, but not 1- to 2-week-old rats. Thus, despite a high abundance in arterial tissue, p38 and p42/44 MAPKs do not regulate contraction of the saphenous artery in the early postnatal period. However, p42/44 MAPK activity contributes to arterial contractions in adult rats.


2021 ◽  
Vol 22 (11) ◽  
pp. 5773
Author(s):  
Maide Ozen ◽  
Yuma Kitase ◽  
Vikram Vasan ◽  
Christopher Burkhardt ◽  
Sindhu Ramachandra ◽  
...  

Chorioamnionitis (CHORIO), placental insufficiency, and preterm birth are well-known antecedents of perinatal brain injury (PBI). Heme-oxygenase-1 (HO-1) is an important inducible enzyme in oxidative and inflammatory conditions. In the brain, HO-1 and the iron regulatory receptor, transferrin receptor-1 (TfR1), are known to be involved in iron homeostasis, oxidative stress, and cellular adaptive mechanisms. However, the role of HO pathway in the pathophysiology of PBI has not been previously studied. In this study, we set out to define the ontogeny of the HO pathway in the brain and determine if CHORIO changed its normal developmental regulation. We also aimed to determine the role of HO-1/TfR1 in CHORIO-induced neuroinflammation and peripheral inflammation in a clinically relevant rat model of PBI. We show that HO-1, HO-2, and TfR1 expression are developmentally regulated in the brain during the perinatal period. CHORIO elevates HO-1 and TfR1 mRNA expression in utero and in the early postnatal period and results in sustained increase in HO-1/TfR1 ratios in the brain. This is associated with neuroinflammatory and peripheral immune phenotype supported by a significant increase in brain mononuclear cells and peripheral blood double negative T cells suggesting a role of HO-1/TfR1 pathway dysregulation in CHORIO-induced neuroinflammation.


2021 ◽  
pp. 8-12
Author(s):  
A.G. Reznikov

The review highlights current views and hypotheses on the pathogenetic role of natural and xenoestrogens in the disorders of programming of neuroendocrine regulation of reproduction, alaptation, and various forms of instinctive behavior (reproductive, eating, parental, etc.) in the perinatal period of development of the female brain. Catecholestrogens, which are formed in the brain as a result of sequential metabolic conversions of testosterone, are involved in exogenous or endogenous androgen-induced defeminization of hypothalamic control of ovulation in early female ontogenesis. In the research on female animals with a knocked out gene of alpha-fetoprotein, the protective role of this protein against the possible pathogenic effect of placental estrogens on the developing brain of female fetuses was proved. The damaging effect of phytoestrogens (genistein, coumestrol) in the early postnatal period on the formation of ovulatory cycles has been shown. Evidence from studies in rodents and other animal species, supported by clinical observations, indicate the potential damaging effect of exposure to low levels of environmental xenoestrogens on the developing brain, in particular on its sexual differentiation and the hypothalamic-pituitary-adrenal axis. The potential hazard of the perinatal exposure to low doses of bisphenol A for the formation of estrogen receptors in the hypothalamus and amygdala of the female brain, sexual behavior and ovulation is discussed. Special attention is paid to the possible physiological role of natural estrogens in the formation of the female neuroendocrine system during puberty. It was concluded that in the early stages of female life, estrogens play a different role in the programming of the neuroendocrine system and behavior, depending on the period of individual development.


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