International Journal of Developmental Neuroscience
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Role of glucocorticoids in the chromaffin‐neuron developmental decision Abstract Chromaffin cells and sympathetic neurons develop from a common neural crest‐derived progenitor cell. The developmental fate of this cell differs depending upon whether it migrates to the sympathetic ganglion or to the adrenal gland primordium, suggesting that local environmental signals control its differentiation. Glucocorticoid (GC) is a good candidate for an important adrenal environmental signal. These steroids are known to regulate PNMT, an adrenal‐specific enzyme. However, in vivo observations suggest that the adrenal microenvironment influences the phenotype of sympathoadrenal progenitor cells as early as E14.5, 2 days before PNMT is first expressed by developing chromaffin cells. Using cDNA probes, we find that GC receptor mRNA can be detected in the embryonic adrenal at least one full day before the initial appearance of PNMT mRNA. This observation is compatible with the idea that the apparent early influence of the adrenal microenvironment reflects the action of GC on progenitors which have migrated into this environment. In support of this, we show that similar influences can be exerted by GC on PC12 cells, which contain GC receptor mRNA but do not express or induce PNMT mRNA. Taken together, these data suggest that other factors in addition to the presence of the GC receptor may be necessary for the developmental appearance of PNMT expression.
International Journal of Developmental Neuroscience - Tập 7 - Trang 475-483 - 1989
Neuronal cell death in the arcuate nucleus of the medulla oblongata in stillbirth Abstract The hypothesis that unexplained stillbirth arises in a similar manner as the sudden infant death syndrome (SIDS) is based in part on shared neuropathologic features between the two entities, including hypoxic‐ischemic lesions such as white matter and brainstem gliosis, as well as aplasia or hypoplasia of the arcuate nucleus on the ventral surface of the medulla. The arcuate nucleus is the putative homologue of the respiratory chemosensory region at the ventral medullary surface in animals that is involved in central chemosensitivity. To determine arcuate nucleus pathology in stillbirth, and its co‐occurrence with evidence of hypoxia‐ischemia, we reviewed brain specimens from the archives of our hospitals from 22 consecutive stillbirths from 22 to 41 gestational weeks. Explained causes of death (n = 17) included nuchal cord, acute chorioamnionitis, placental abruption, and fetal glomerulosclerosis; 5 cases were unexplained. In 12 brains, we observed nuclear karyorrhexis and/or pyknosis with cytoplasmic hypereosinophilia in neurons in the arcuate nucleus in both explained (n = 8) and unexplained (n = 4) cases (54.5% of total cases). Three additional cases had arcuate aplasia (n = 1) or hypoplasia (n = 2) (13.6% of total cases); one of the latter cases also had neuronal necrosis in the hypoplastic arcuate. The degree of gliosis in the region of the arcuate nucleus was variable across all cases, without statistically significant differences between groups with and without arcuate nucleus necrosis. Other lesions in association with (n = 14) and without (n = 8) arcuate nucleus abnormalities were diffuse cerebral white matter gliosis, periventricular leukomalacia (PVL), and neuronal necrosis in the hippocampus, basal ganglia, thalamus, basis pontis, and brainstem tegmentum. In 16/20 (80.0%) cases (with or without histologic necrosis of the arcuate), immunostaining with caspase‐3 demonstrated positive neurons. Our findings suggest that neuronal pathology in the arcuate nucleus may be both developmental (13.6%) and acquired (54.5%). The association of neuronal necrosis and apoptosis in the arcuate nucleus with systemic entities involving fetal ischemia, and with other brain lesions consistent with ischemia, e.g., cerebral white matter gliosis, suggests that ischemia plays a role in the arcuate nucleus damage as well. Thus, the underpopulation of arcuate neurons detected postnatally in some SIDS infants may be secondary to an acquired insult in mid‐ or late gestation, and in other cases, a primary developmental lesion in early gestation, or both. The role of arcuate nucleus pathology in the pathogenesis of fetal demise remains to be determined.
International Journal of Developmental Neuroscience - Tập 26 - Trang 133-140 - 2008
Free radical scavenging systems in developing rat brain Abstract Because the developing brain is subject to high oxygen tension and lacks a functional blood‐brain barrier, anti‐oxidant protection is important to development in the brain. The levels of superoxide dismutase, copper‐zinc superoxide dismutase. manganese superoxide dismutase. catalase, glutathione and related enzymes, namely, glutathione reductase and glutathione peroxidase were determined in rat brain at various stages of development. The levels of thiobarbituric acid reactive products, indicative of lipid peroxidation, were very low at birth and increased to adult levels by the 16th day after birth. Brain glutathione levels displayed significant variations during the first 2 weeks after birth but not thereafter. Catalase activity in developing brain slowly increased over 45 days. Total superoxide dismutase activity in 1‐day‐old rat brain, 80% of the adult rat brain level, subsequently decreased on day 6. Total superoxide dismutase activity, however, increased again in 10‐day‐old rats and remained constant thereafter. While the developmental pattern of manganese superoxide dismutase was similar to that of the total superoxide dismutase, the copper‐zinc superoxide dismutase levels were low at birth and reached adult levels on the 10th day after birth. There was no variation in glutathione reductase and peroxidase levels except for a decrease on day 16 of glutathione reductase and slow increase in adult levels by day 28. The present findings suggest that the overall levels of antioxidant enzymes in the developing brain are comparable to a large extent to those present in the adult brain. In contrast to the developing brain, hepatic levels of glutathione, total superoxide dismutase, manganese superoxide dismutase are significantly lower at birth and increase during development.
International Journal of Developmental Neuroscience - Tập 9 Số 2 - Trang 181-185 - 1991
Different degradation rates of junctional and extrajunctional acetylcholine receptors of human muscle cultured in monolayer and innervated by fetal rat spinal cord neurons Abstract It is well demonstrated that in intact animals the degradation rate of the junctional acetylcholine receptor (AChR) is significantly slower than that of the extrajunctional receptor. Such data, however, are not available for human AChRs because the required experimentation cannot be performed in humans. We have now studied the degradation rate of the junctional and extrajunctional AChRs, utilizing our tissue culture model, in which well‐differentiated neuromuscular junctions (NMJs) form on human muscle cultured in monolayer and innervated long‐term by fetal rat spinal cord neurons. Half‐life of AChRs was studied by a method utilizing the autoradiography of 125 I‐αbungarotoxin and computerized video image analysis. Extrajunctional AChRs degraded with a half‐life of 1.3 days whereas junctional AChRs degraded with a half‐life of 3.5 days. Our studies demonstrate for the first time that in innervated cultured human muscle: (a) the life span of human junctional AChR, is approximately 3 times longer than that of the extrajunctional AChR and (b) the stability of human AChR is neuronally regulated. This system can now be applied to evaluate the influence of pharmacologie agents on the stability of human junctional AChR, which is of potential importance in the treatment of myasthenia gravis and other diseases of the NMJ.
International Journal of Developmental Neuroscience - Tập 10 - Trang 37-44 - 1992
The time course of hippocampal cholinergic innervation in the developing hypothyroid rat. A combined histochemical and biochemical study of acetylcholinesterase activity Abstract Development of cholinergic innervation in the hippocampal formation of normal and hypothyroid rats was studied by a combined biochemical and histochemical analysis of acetylcholinesterase (AChE) activity in normal and hypothyroid rats. The normal developmental pattern of cholinergic activity suggests an entrance of septal cholinergic fibers from the fimbria to different zones of the hippocampal formation mainly during the first postnatal week. By 10 days of age, the regional distribution of staining was similar to that in the adult. Thereafter, the intensity of staining increased without major changes in the laminar organization. As shown by closely related histochemical and biochemical findings, hypothyroidism led to a delay in the arrival of cholinergic afferences and a possible subsequent cholinergic hyperinnervation of the hippocampal formation in adulthood. These results are discussed taking into account the time course of structural development in the two synaptic compartments, namely the extrinsic septal neurons and intrinsic pyramidal and granule cells, in comparison with the development of thyroid function.
International Journal of Developmental Neuroscience - Tập 7 - Trang 301-308 - 1989
Thyroid hormone deficiency changes the distribution of oligodendrocyte/myelin markers during oligodendroglial differentiation <i>in vitro</i> Abstract Myelination depends on the proper differentiation of oligodendrocytes and several factors may influence this event. For instance, thyroid hormone (T3) affects the timing of differentiation and regulates the expression of several enzymes involved in the synthesis of complex lipids and in the expression of some myelin structural proteins. We investigated the effect of T3 deficiency on oligodendroglial differentiation and in the distribution of oligodendrocyte/myelin proteins 2′3′‐cyclic nucleotide 3′‐phosphodiesterase (CNPase) and myelin basic protein (MBP). Oligodendroglial‐enriched cultures were obtained from cerebra of neonate rats grown in a modified medium. The T3‐deficient status was induced by using medium devoid of T3. We observed a delay, in T3‐deficient cultures, in oligodendroglial maturation characterized by less extensive processes and membrane vellum than in controls. In control cultures, CNPase immunoreactivity was punctated, showing cell bodies and processes at earlier stages and redistribution to cytoskeleton vein‐like structures in later stages. In T3‐deficient cultures, CNPase remained in a punctated pattern and only at 10 days in vitro we observed CNPase redistribution to the presumptive cytoskeleton vein‐like structures. MBP in control cultures was distributed through the whole cell body and processes whereas in T3‐deficient cultures, MBP immunoreactivity was concentrated in the perinuclear region. These results reinforce the hypothesis that T3 is an important factor in oligodendrocyte differentiation, particularly regarding the distribution of myelin proteins.
International Journal of Developmental Neuroscience - Tập 24 - Trang 445-453 - 2006
Neurotrophins: Role in adverse pregnancy outcome Abstract Proper placental development is essential during pregnancy since it forms the interface between the maternal–foetal circulations and is critical for foetal nutrition and oxygenation. Neurotrophins such as nerve growth factor (NGF), brain derived neurotrophin (BDNF), neurotrophin‐3 (NT‐3) and neurotrophin‐4/5 (NT‐4/5) are naturally occurring molecules that regulate development of the placenta and brain. BDNF and NGF also involved in the regulation of angiogenesis. Recent studies suggest that the levels of BDNF and NGF are regulated by docosahexaenoic acid (DHA) which is an important omega‐3 fatty acid and is a structural component of the plasma membrane. Oxidative stress during pregnancy may lower the levels of DHA and affecting the fluidity of the membranes leading to the changes in the levels and expression of BDNF and NGF. Therefore altered levels and expression of NGF and BDNF may lead to abnormal foetal growth and brain development that may increase the risk for cardiovascular disease, metabolic syndromes and neurodevelopmental disorders in children born preterm. This review discuss about the neurotrophins and their role in the feto‐placental unit during critical period of pregnancy.
International Journal of Developmental Neuroscience - Tập 37 - Trang 8-14 - 2014
Malic enzyme activity in the developing rat brain in relation to thyroid status Abstract Malic enzyme activity in the soluble fraction of neonate brains from mothers fed with propylthiouracil (0.015% w/v) in drinking water from day 12 of the gestation period was significantly lowered (P < 0.01 ) as compared to the offspring of normal mothers. Supplementation of triiodothyronine to the neonates from experimental mothers restored the malic enzyme activity to normal levels. However, administration of triiodothyronine to adult control rats did not influence malic enzyme activity in the brains of these animals. Our data suggest that during the initial critical period of brain maturation, malic enzyme is under the control of thyroid hormones. The response of malic enzyme towards thyroid hormones is lost once the brain has matured.
International Journal of Developmental Neuroscience - Tập 7 - Trang 203-208 - 1989
Postnatal maturation of brain cholinergic systems in the precocial murid <i>Acomys cahirinus</i>: Comparison with the altricial rat Abstract The spiny mouse (Acomys cahirinus ) is the only precocial murid species. It has some neuroanatomical peculiarities such as a relatively thin cerebral cortex and a large hippocampus. The levels of choline acetyltransferase. membrane‐bound acetylcholinesterase and muscarinic receptor sites (measured as [3 H]quinuclidynil benzilate binding) were assessed in the whole brain on days 1, 7, 14, 21, 28 and 80 (adult), and compared with those of Wistar rats of the corresponding ages. At birth choline acetyltransferase was significantly higher in spiny mice than in rats but the adult levels were similar, with an overall increase of about 5.2‐ and 14‐fold for the former and the latter species, respectively. Membrane‐bound acetylcholinesterase level and maximal density of muscarinic receptor sites in spiny mice were considerably higher at birth, in contrast adult levels were significantly lower than in rats with a respective overall increase of about 1.5‐ and over 4.5‐fold. The high degree of maturity attained at birth by spiny mice partially depends on the long gestation period. However, if we consider postconception age, the maturation of choline acetyltransferase appears to be delayed at birth in the spiny mice, probably in relation to the lack of external stimulation during intrauterine life. In the cerebral cortex, hippocampus and striatum of adult spiny mice, when compared with the rats, there were similar levels of choline acetyltransferase but lower levels of membrane‐bound acetylcholinesterase and, in the cerebral cortex, lower density of muscarinic receptor sites.
International Journal of Developmental Neuroscience - Tập 4 - Trang 375-382 - 1986
Maternal vitamin D depletion alters neurogenesis in the developing rat brain Abstract Evidence is accumulating that normal levels of vitamin D are important for brain development. Vitamin D acts as an anti‐proliferative agent in a wide variety of tissues and developmental vitamin D (DVD) deficiency has been shown to alter brain structure and function. The aim of this study was to investigate the effect of DVD deficiency on neuroprogenitor formation in the neonatal brain. We show that DVD deficiency increased the number of neurospheres formed in cultures from the neonatal subventricular zone. Exogenous vitamin D added to the culture medium reduced neurosphere number in control but not DVD cultures. We show the receptor for vitamin D is concentrated in the subventricular zone and is also present in cultured neurospheres prepared from this region. These results show that vitamin D can regulate cell proliferation in the developing brain. Further studies are warranted to examine the underlying mechanisms for these findings.
International Journal of Developmental Neuroscience - Tập 25 Số 4 - Trang 227-232 - 2007
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