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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Anatomy and embryology 156 (1979), S. 73-88 
    ISSN: 1432-0568
    Keywords: Closure ; Development ; Mammalina embryo ; Neural tube ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The fusion of the neural walls in the cephalic part of mouse embryos varying in age from 9 to 20 somites was examined with the electron microscope. In the rhombencephalic region the rim of the neural wall was formed from outside inward by ectodermal surface cells, a row of flattened cells without surface projections and neuroepithelial cells. At the junction of the surface ectoderm and the flat cells were seen large projections containing a cytoplasmic matrix without organelles and previously referred to as “ruffles”. The initial contact between the walls was made by the large cytoplasmic arms and numerous finger-like projections interdigitating with similar projections from the opposite wall. The projections originated from the surface ectoderm and possibly neural crest cells. During further fusion the surface ectoderm cells formed dense membrane specializations, thus establishing a firm contact. The initial contact in the mesencephalon was formed by extensions from the surface ectoderm and was followed by the formation of specialized membrane junctions, as seen between the surface ectoderm in the rhombencephalon. The neuroepithelial cells facing the gap between the neural walls with their apical ends made contact with the cells from the opposing wall by numerous finger-like projections but membrane specializations failed to develop. The closing mechanism in the prosencephalon and anterior neuropore regions differed from the previous areas in that the initial contact was established by the neuroepithelial cells. Only after this contact had been formed did the surface ectoderm cells close the gap. In contrast with the other areas many phagocytosed particles were seen in the prosencephalon and in the region of the anterior neuropore. Many particles from degenerated cells were found inside healthy surrounding cells. Some of these particles contained nuclear material and cytoplasmic organelles.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Anatomy and embryology 159 (1980), S. 223-234 
    ISSN: 1432-0568
    Keywords: Vitamin A ; Neural tube closure ; Exencephaly ; Anencephaly
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of excess vitamin A on the closure of the neural tube in mouse embryos was examined with light microscopy, transmission and scanning electronmicroscopy. The embryos were treated with the vitamin just before closure of the brain vesicles and examined during the following 24 h, a period during which under normal conditions the brain completely closes. At 18–24 h after treatment the external features of the treated specimens began to differ from those of the controls. In the treated embryos the neural walls folded laterally and became widely separated, whereas those of the controls folded dorsomedially and fused in the midline. Histologically, the first difference between treated and control embryos was noted at two hours after treatment, when large intercellular spaces appeared between the neuroepithelial cells of the treated embryos. These spaces were mainly present between the apical ends of the wedge-shaped neuroepithelial cells. This accumulation of intercellular spaces interfered with the normal morphogenetic movement of the neural walls, which remained convex instead of becoming concave. This convex bending resulted in non-closure of the neural tube. In addition to the appearance of large intercellular spaces some neuroepithelial cells as well as some mesenchymal, endothelial, and surface ectoderm cells showed swelling and degeneration as a result of the vitamin A treatment. This cell degeneration probably contributes to failure of the neural tube to close due to loss of cohesion at the luminal surface and the lack of mesenchymal support needed for the elevation of the neural walls. However, the increase of intercellular spaces at the apical side of the neuroepithelium is in all probability the major cause for the failure of the neural tube to close.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 189 (1977), S. 625-639 
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: In mouse embryos varying in age from 9 to 20 somites the first closure of the neural groove was found to occur in the cervical region. The fusion process gradually proceedéd in rhombencephalic direction until it reached a level just caudal to the otic pits. Shortly afterwards the prosencephalic walls fused together independent of the rhombencephalic closure. This prosencephalic fusion process proceeded caudally in the direction of the mesencephalon until it reached the rostral portion of the rhombencephalon. In this region the two independent fusion processes met each other. In addition the prosencephalic fusion proceeded in rostral direction toward the anterior neuropore, which was the last part of the brain vesicles to close. Hence, the closure of the brain vesicles is not a zipper-like process proceeding from the rhombencephalon to the anterior neuropore, but occurs at several places at the same time and proceeds in a rostral as well as in a caudal direction.At the cellular level considerable differences in the fusion process were found to exist between the various brain vesicles. In the rhombencephalon the first bridge between the two opposing walls was formed by surface ectoderm and neural crest cells. In the mesencephalon single squamous ectoderm and a few neuroepithelial cells established the first contact, whereas in the prosencephalon the apical ends of several neuroepithelial cells fused together to overbridge the gap between the opposing walls. The surface ectoderm cells subsequently covered the neuroepithelial bridge. In the region of the anterior neuropore the fusion was similar to that between the prosencephalic walls, the only difference being that in the anterior neuropore area many more darkly stained particles indicating cell degeneration, were present than in the prosencephalon. It is thus concluded that considerable differences exist in the fusion of the neural walls between the various brain vesicles.
    Type of Medium: Electronic Resource
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