Browsing by Subject "NEUROLOGICAL FUNCTION"

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    Neural tissue continues its maturation at the site of neural tube closure defects
    (SPRINGER-VERLAG) Selçuki, M; Vatansever, S; Inan, S; Sanci, M; Sayhan, S; Bagdatoglu, C
    Objective. Our objective was to investigate the relation between the embryological development and neural tissue maturation at the site where the neural plate failed to form a neural tube. Material and methods. Samples from 15 aborted human fetuses with neural tube defects (NTD). All of the fetuses were between 20 and 25 gestational weeks old. Indicators of neural tissue maturation, formation of basal lamina, expression of integrins and neuron specific class III beta tubulin (tuj1) were investigated. To detect the adverse effects of the environment, if any, p53 and bcl-2 activity at both sites of the open and closed neural plate were investigated as well. Results. No difference was found in the expression of maturation-related molecules at the site of the neural plate that remained open compared with the site where the neural tube is normally formed. While high p53 activity was noted in neural tissue at the site of the neural tube defect, no such activity was detected in the neural tissue where the neural tube is normally formed. Conclusion. Our results suggested that maturation and differentiation of neural tissue continued regardless of the failure of neural tube closure. Therefore, the neurological deficits that are encountered in NTD patients should be related to secondary damage such as amnion fluid toxicity, uterus contractions, labor, etc. It seems valuable to save the neural plate before the negative effects of the environment renders the neural tissue functionless.
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    The curly tail mouse model of human neural tube defects demonstrates normal spinal cord differentiation at the level of the meningomyelocele
    (SPRINGER-VERLAG) Selçuki, M; Manning, S; Bernfield, M
    The paralysis associated with lumbosacral meningomyelocele has been attributed both to myelodysplasia and to degeneration of the exposed neural tissue. Surgically created dysraphism shows that exposure of an intact spinal cord in a genetically normal animal results in degeneration of the normal nervous tissue and subsequent paralysis. Our objective was to study neuronal differentiation in the curly tail mouse mutant model, which develops lumbosacral meningomyelocele naturally and is a phenocopy of nonsyndromic human neural tube defects. Prenatal repair of meningomyelocele assumes that the normal neuronal differentiation program occurs despite failure of neurulation. Here we demonstrate that this most suitable animal model has normal differentiation of neuronal structures at the level of the meningomyelocele. TuJ1, an antibody to neuronal specific class III beta -tubulin, an early marker of neuronal differentiation, was used to stain paraffin-embedded sections of curly tail mouse embryo meningomyelocele. Embryos were examined at embryonic day 13.5 (E13.5). The inbred mouse strain, C57BL6/J, which is genetically similar to the curly tail mouse, was used as a control in these studies. We show that early neuronal differentiation appears intact within the meningomyelocele. TuJ1 stains structures within the open neural tube. Motor neurons are present in the ventral horn and ventral roots. Dorsal root ganglia are present and of similar size to controls. The staining pattern is similar to that seen in the C57BL/6J control mouse, although dorsal structures are laterally displaced in the curly tail meningomyelocele. Based on this model, fetal surgery to repair human meningomyelocele may preserve neurological function in those cases where there is not an inherent genetic defect of the neural tissue.