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At least 19 recordsLinked to original sources

PubMed1992

Exogenous transferrin is taken up and localized by the neurulation-stage mouse embryo in vitro.

We have screened neurulation-stage mouse embryos for regional differences in protein distribution, by two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The screen has revealed an 83-kD protein (pI 6.8) that is present in embryo regions where neurulation is in progress but not in regions where neurulation is complete. The 83-kD protein is not synthesized in the neurulation-stage embryo or in the yolk sac, but is taken up from the culture serum in vitro and, probably, from the maternal serum in utero. The 83-kD protein has been identified as transferrin on the basis of its electrophoretic migration and recognition on Western blots by an antitransferrin antibody. Culture of embryos in serum containing 125I-transferrin, followed by autoradiography of embryo sections, shows that transferrin is taken up and localized in the gut beneath the closing neural folds at several levels of the body axis in 8.5- and 9.5-day embryos. In situ hybridization studies show that the transferrin receptor mRNA is expressed in all cells of the 9.5-day embryo, including the gut endoderm. These findings are consistent with a role for transferrin in development of the gut and perhaps, indirectly, in completion of neurulation during early mouse embryogenesis.

Animals↗

PubMed1979

Cephalic neurulation and optic vesicle formation in the early mouse embryo.

The overall pattern of cephalic neurulation and the concomitant early development of the optic vesicles in mouse embryos were examined by scanning electron microscopy. Paraffin-sectioned specimens were also examined. The overall pattern of closure of the cephalic neural folds accords well with earlier observations of this process. The earliest indication of optic placode formation was seen in histological sections of embryos at the 4-somite stage, while optic pit formation was first observed at the 5- to 6-somite stage. The upper halves of the optic vesicles were formed in 10- to 15-somite embryos by the fusion of the neural folds at the junction between the mesencephalon and prosencephalon, while closure of the lower halves was associated with the closure of the rostral neuropore, and was usually completed by about the 20-somite stage. By the 25- to 30-somite stage, a rapid increase in the volume of the forebrain was observed, so that the optic vesicles were displaced laterally. An overall increase in the volume of the optic vesicles and decrease in the diameter of the optic stalks were also observed at this time. This account of cephalic neurulation and optic organogenesis provides useful baseline data relevant to the study of the normal early development of the mouse. A comparison is made between similar events in the rat, the hamster, and the human embryo.

Animals↗

PubMed1992

Morphological and mapping studies of the paranodal and postnodal levels of the neural plate during chick neurulation.

The morphology of the paranodal and postnodal levels of the neural plate as well as the fate of its cells was examined in chick embryos at stages 3-11. The morphology of the paranodal and postnodal levels of the neural plate closely resembles that of the prenodal neural plate. Furthermore, during shaping and bending of the neural plate, these levels undergo changes similar to those of the prenodal level. In short, the paranodal and postnodal levels of the neural plate consist of a pseudostratified columnar epithelium that thickens dorsoventrally and narrows mediolaterally and then undergoes localized furrowing and folding. Fate mapping revealed that at mid-neurula stages, the prospective hindbrain and spinal cord levels of the neuraxis flank the primitive streak. Hensen's node moves caudally with respect to these future neuraxial levels as it regresses during the latter stages of gastrulation. Cells of the medullary cord, the rudiment of the secondary portion of the neural tube, arise in the vicinity of the cranial portion of the primitive streak, near the caudal end of the postnodal levels of the neural plate. Thus, during stages of gastrulation and primary neurulation, the precursor cells of the primary and secondary portions of the neural tube (spinal cord) lie in close proximity to one another. This study provides new information on the morphology and extent of the paranodal and postnodal levels of the neural plate, the changes these areas undergo during shaping and bending of the neural plate, and the contributions of its cells to the primary and secondary levels of the neural tube, increasing our understanding of the complex events underlying avian gastrulation and neurulation.

Animals↗

PubMed1976

A scanning electron microscopic and flame spectrometry study on the role of Ca2+ in amphibian neurulation using papaverine inhibition and ionophore induction of morphogenetic movement.

SEM observations reveal that papaverine, which interferes with Ca2+ flux, inhibits neural fold formation causing a flattening of the cellular surface and a broadening of cellular junctions. Ionophore A23187 and EGTA both counter this effect promoting a rapid cellular constriction which results in the formation of neural ridges and folds as individual cells become uplifted and ruffled. Flame spectrometry data indicate that as Ambystoma maculatum or mexicanum embryos neurulate Ca2+ is released to the medium, a condition which is impeded by papaverine. Ionophore A23187 induces Ca2+ influx whereas EGTA induces an efflux. Since both agents affect similar morphological changes it is suggested that the availability of free Ca2+ is crucial in controlling the morphogenetic movements of neurulation. It is now apparent that neuro-axial development in the urodele is accompanied by a Ca+2 efflux, but the mechanism(s) responsible for the ion's release is unknown.

Ambystoma↗

PubMed1975

An ultrastructural examination of the role of cell membrane surface coat material during neurulation.

Data from neural crest cultures indicate that cell surface coat material (CSM) is directly involved in cellular migration and events surrounding differentiation. To investigate whether the CSM also has a morphogenetic role, embryos of the amphibian Ambystoma maculatum were examined ultrastructurally throughout the stages of neurulation. Segments of the neural axis were fixed in glutaraldehyde-containing Alcian blue 8GX, which reportedly enhances preservation of CSM, and were postfixed in OsO4 containing 1 percent lanthanum nitrate, which stains the CSM. The medial groove formed by the appearance of the neural ridges contains a large amount of CSM and numerous vesicles coated with lanthanum-positive material. In contrast, the lateral ridge surfaces are covered by a small amount of uniformly distributed CSM and a paucity of vesicles. As the ridges begin to fold there is a progressive increase in the amount of CSM within the presumptive neural tube region. Further convergence of the neural folds is accompanied by an increase of CSM at their leading edges. As the folds approximate each other, lanthanum-positive material physically bridges the gap. However, as the apposing tissue actually abuts to form the neural tube, no CSM is observed in the remaining interspace. The specific distribution and sequential accumulation of cell CSM during the events of neurulation strongly suggest its direct participation in the morphogenetic process.

Ambystoma↗

PubMed1979

Embryotoxicity of arsenic acid: light and electron microscopy of its effect on neurulation-stage rat embryo.

To clarify the light and electron microscopic changes accompanying embryonic death from a lethal dose of arsenic acid, MP 1 pregnant rats were injected i.p. with 30 mg/kg arsenic acid at 1:30 p.m. on day 9 of gestation (the neurulation stage). At 4 hours after treatment, some cell necrosis occurred in the neuroectoderm and the mesoderm of the embryo. At six hours later, cell necrosis increased in the neuroectoderm and the mesoderm, whereas those in the surface ectoderm and the endoderm were very few. In the embryo 12 hours after treatment, abnormal mitotic cells exhibiting vesiculation of the endoplasmic reticula, and abnormal interphase cells characterized by the ring-shaped nucleoli in the nucleus and the enlargement of cisternae of the endoplasmic reticula and the nuclear envelope, were observed in the neuroectoderm and the mesoderm. Debris from cell necrosis and the said abnormal mitotic and interphase cells were ejected from the neuroectoderm into the amniotic coele. In the embryo 24 hours later, neurulation was stopped and the V-shaped neural fold remained. The somite formation was retarded. The surviving cells in the embryo sometimes contained phagocytic vesicles in the cytoplasm, but no other anomalies were encountered. It was considered that a variety of metabolic reactions may be disturbed by arsenic acid, resulting in numerous cell necrosis and abnormal mitotic and interphase cells in the neuroectoderm and the mesoderm of the rat embryo.

Animals↗

PubMedDate not supplied

[The morphogenesis of the human brain on the 27th-35th day of development with disordered neurulation].

Human embryos with anomalies of brain and spinal cord were studied on 27-35th day of the development. It was established that developmental anomalies were associated with the disturbed formation of neural tube. The reconstruction of three-dimensional brain arrangement of embryos has shown the presence of different variants of nonclosed medullar tori. In mild disturbance of neurulation, there is an acceleration of organogenesis and morphological differentiation induced by the shackening of normal mechanical tensions and relaxation of neuroepithelial layers. In presence of substantial parts of open neural tube, the development of brain and ectodermal derivatives becomes disturbed to be a possible cause of anencephaly and hypotelorism. The type of disturbed neurulation inducing developmental anomalies of nervous system is suggested to be a factor which determines forms of secondary craniofacial and cranial pathology.

Abortion, Spontaneous↗

PubMed1990

Vimentin and keratin are expressed in the neurogenic tissue of the rabbit embryo during primary neurulation.

Against the commonly held belief that differential expression of keratins is a sign of neurogenic commitment amongst ectodermal cells of the early vertebrate embryo we show here that the same keratins (8 and 18) are expressed in the epidermal ectoderm and the neurectoderm throughout primary neurulation of the early rabbit embryo, i.e. between 8.5 and 11 days post conceptionem (d.p.c.). However, keratin expression decreases during this developmental period and, by the time primary neurulation is completed, keratin expression is virtually absent in the cells of the neural tube. Vimentin expression is weak, at first, but increases in a reciprocal manner as compared to the decreasing keratin expression until it has reached a high and stable level of expression in the established neural tube of the 10 to 11 day old rabbit embryo.

Animals↗

PubMed1991

Cell movements driving neurulation in avian embryos.

Neurulation, formation of the neural tube, a crucial event of early embryogenesis, is believed to be driven by the coordination of a number of diverse morphogenetic cell behaviors. Such behaviors include changes in cell number (division, death), cell shape and size (wedging, palisading and spreading), cell position (rearrangement or intercalation) and cell-cell and cell-matrix associations (including inductive interactions). The focus of this essay is on epiblast cell movements and their role in shaping and bending of the neural plate. Neurulation is a multifactorial process requiring both intrinsic (within the neural plate) and extrinsic (outside the neural plate) forces. The origin and movements of three populations of epiblast cells have been studied in avian embryos by constructing quail/chick transplantation chimeras and by labeling cells in situ with identifiable, heritable markers. MHP (median hinge-point neurepithelial) cells originate principally from a midline epiblast area rostral to and overlapping Hensen's node. In addition, a few caudal MHP cells originate from paranodal epiblast areas. MHP cells stream down the length of the midline neuraxis in the wake of the regressing Hensen's node. This streaming occurs as a result of cell division (presumably oriented so that daughter cells are placed into the longitudinal plane rather than into the transverse plane) and rearrangement (intercalation), resulting in a narrowing of the width of the MHP region with a concomitant increase in its length. L (lateral neurepithelial) cells originate from paired epiblast areas flanking the rostral portion of the primitive streak, and they stream down the length of the lateral neuraxis concomitant with regression of Hensen's node.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1976

Topographical changes along the neural fold associated with neurulation in the hamster and mouse.

The topography of the ectoderm was examined by scanning electron microscopy during neurulation in hamster and mouse embryos. Stages from the appearance of the neural folds to closure of the posterior neuropore were studied. Progressive development of a zone of altered cellular morphology was observed along the crests of the neural folds. This zone evolved from an abrupt transition between surface and neural regions of the ectoderm to a narrow band of flattened cells which exhibited numerous membranous "ruffles" in the mouse, or blebs and presumably degenerating cells in the hamster, immediately prior to contact between the folds. These alterations were more prominent along the anterior than the posterior portions of the folds. Contact of the folds occurred first between the flattened cells with subsequent union of the surface cells. Stages of neural crest cell formation was observed subjacent to the zone of alterations in histological sections. It is suggested that the observed surface alterations may reflect changes in the membrane properties of the altered cells which are correlated with both neural crest formation and initial adhesion between the folds.

Animals↗

PubMed1992

Mesoderm movement and fate during avian gastrulation and neurulation.

Quail/chick transplantation chimeras were constructed during stages of gastrulation and neurulation to follow the subsequent movement and fate of cells of the primitive streak. All grafts were placed solely within the confines of the primitive streak to prevent confusion between cells that had not yet ingressed and those that had already ingressed, and transplanted cells were distinguished from host cells on the basis of a naturally occurring cell marker. Pathways of movement of ingressing cells corresponded to their level of residence within the primitive streak. Cells residing within Hensen's node (the cranial end of the primitive streak) initially migrated mainly cranially, remaining on or near the midline, and then extended caudally along the midline as regression of Hensen's node occurred. Cells residing within the nodus posterior (the caudal end of the primitive streak) migrated caudally. Cells residing at levels of the primitive streak between Hensen's node and the nodus posterior typically migrated bilaterally, confirming that such cells had not already ingressed prior to their transplantation (in which case, they would have migrated unilaterally). Subsets of these cells residing at progressively more caudal levels of the primitive streak migrated incrementally more laterally. Hensen's node contributed cells to the gut endoderm, head mesenchyme, notochord, and median hinge-point (MHP) cells of the neural tube (future floor plate). At younger stages (i.e., stages 3a, 3b) Hensen's node contributed cells to principally the foregut endoderm and head mesenchyme, whereas at older stages (i.e., stages 3c, 3d, 4), it contributed cells to principally the notochord and MHP region. The remaining segments of the cranial half of the primitive streak contributed cells to the various mesodermal subdivisions of the embryo, and the lengths of the segments forming these subdivisions were estimated. The most cranial level of the streak (directly behind Hensen's node) contributed cells to the most medial mesodermal subdivisions (head mesenchyme, somites) and consecutively more caudal levels of the streak contributed cells to sequentially more lateral mesodermal subdivisions (intermediate mesoderm, lateral plate mesoderm). The caudal half of the primitive streak contributed cells to the extraembryonic mesoderm, with the nodus posterior contributing to the most caudal extraembryonic mesoderm, including the blood islands. Our results confirm and extend the previous avian prospective fate maps, increasing our understanding of the movement and fate of cells of the gastrula and neurula stages.

Animals↗

PubMed1992

Positional control of mesoderm movement and fate during avian gastrulation and neurulation.

Segments of primitive streak from donor quail embryos at stages of gastrulation and neurulation were transplanted heterotopically and isochronically to primitive streaks of host chick embryos. The subsequent movement and fate of grafted cells was determined using the quail nucleolar marker to define grafted cells. The pattern of movement of grafted cells depended on their new position within the primitive streak, not on their original position. When cells of cranial regions were placed more caudally, they moved to mesodermal subdivisions that were located lateral to those they would have populated if left in their original position. When caudal segments were placed more cranially, they moved to more medial mesodermal subdivisions. Whether the fate of grafted cells corresponded to their original location or their new location depended on both their level of origin and their new position. Cells from heterotopically transplanted Hensen's nodes, which migrated to the somitic and more lateral mesoderm, self-differentiated notochords. Similarly, in some cases, heterotopically transplanted prospective somitic cells, which migrated to lateral plate mesoderm, formed ectopic somites. In other cases, however, grafted cells contributed to the host's somites, intermediate mesoderm, and lateral plate mesoderm. Moreover, prospective somitic cells, which migrated to the extraembryonic lateral plate mesoderm, changed their fate and formed extraembryonic lateral plate mesoderm; and prospective lateral plate mesoderm cells, which migrated to the somitic mesoderm, formed somites as well as intermediate mesoderm and lateral plate mesoderm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

Distribution of surface coat material on fusing neural folds of mouse embryos during neurulation.

Fusing and non-fusing regions of neural folds from mouse embryos were examined during neurulation for the distribution of extracellular macromolecules (surface coats) prior to and at the time of closure. Ruthenium red staining of 10th day ICR/DUB mouse embryos was used to detect the distribution of surface coat material. Light microscopic examination of fusing and non-fusing regions in the midbrain, hindbrain, and spinal cord showed a consistent increase in ruthenium red positive material immediately prior to closure. Heavy deposits of positive staining material were present along apical neural fold borders and overlying ectoderm cells. This staining pattern was consistent in the three regions examined, but the pattern of initial contact between opposing neural folds differed. In mid- and hindbrain areas contact was initiated by overlying ectoderm, whereas in spinal cord regions contact was first established by neuroepithelial cells. Once contact between opposing neural folds was initiated a decrease in stainable material was observed.

Animals↗

PubMed1992

Comparison of staging systems for the gastrulation and early neurulation period in rodents: a proposed new system.

Because there is no standard developmental staging system for the early postimplantation period of rodent embryos, investigators must now choose between a variety of systems that differ significantly. We have reviewed many of these staging systems and have summarized the ambiguities within them and the inconsistencies among them. In order to compare systems, we first obtained a consensus of the order of developmental events from the literature, and then attempted to fit existing systems into this order taking into account inconsistencies in terminology and blurred borderlines between stages. We were able to do this for most systems but not all because some were too divergent. We found that inconsistencies in definition of some terms, such as "primitive streak stage" and those used to describe the early neurulation process (neural plate, neural groove, neural folds, and head fold) cause much confusion. In order to develop an unambiguous system which can be used by all investigators, we propose to modify Theiler's system, which is one of the most commonly used systems but is not defined precisely during the early postimplantation period. We suggest making subdivisions of the original stages as follows: 1) stage 8 into 8a and 8b, by the degree of extension of the proamniotic cavity into the extraembryonic region; 2) stage 10 into 10a and 10b, by the completion of amnion formation; 3) stage 11 into 11a, 11b, and 11c, by the appearance of neural folds and foregut pocket. After Stage 12, the number of somite pairs can be used to precisely stage embryos.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Deceleration and acceleration in the rate of posterior neuropore closure during neurulation in the curly tail (ct) mouse embryo.

Curly tail (ct) is a mouse mutant producing spinal neural tube defects as a result of delayed closure of the posterior neuropore (PNP). The purpose of the present study was to determine in ct/ct embryos the time of onset of the delay in PNP closure, and the pattern of this closure, as well as to study the possibility that reopening of the neural tube occurs. Normal spinal neurulation was studied in non-mutant Swiss (Sw) embryos. In the latter, the average PNP length diminished steadily between the 7- and 25-somite stages, and then decreased more rapidly, indicating an acceleration of closure rate, until the 30- to 32-somite stage, when all PNPs closed. PNP width decreased steadily between the stages of 7 and 30 somites. In ct/ct embryos the average PNP length showed a slight increase between the stage of 23 to 28 somites, indicating a temporary deceleration of closure rate, and the range of PNP sizes increased markedly. This was followed by a decrease in PNP length until the 37-somite stage, indicating an acceleration of closure rate. From the stage of 32 somites onwards, the proportion of embryos with closed PNPs gradually increased to 90%. The population of ct/ct embryos was subdivided. Embryos with large PNPs showed a marked deceleration of closure rate during a period of 11 somite stages, followed by a brief but very high acceleration of closure rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

The masking effect of sialic acid on Con A, PNA and SBA ectoderm binding sites during neurulation in the bantam chick embryo.

The masking effect of sialic acid on cell surface carbohydrates localized on the ectoderm in stage 6-11 bantam embryos was examined using fluorescein isothiocyanate-labeled Con A, PNA, SBA, LFA, and LPA before and after neuraminidase treatment. The results showed selective lectin binding on both the neuroectoderm and the surface ectoderm. In general, these lectin-binding sites increased or were at least expressed on neuroectoderm during neurulation. On the apical surfaces of the developing neuroectoderm, masked Con A-binding sites were evident from the earliest stage and rapidly increased. These sites coexisted with unmasked binding sites which gradually increased. Masked PNA sites were rarely observed but became abundant in later stages, even though coexistent unmasked sites also rapidly increased. Masked SBA sites were poorly observable in the early stage and gradually increased thereafter, whereas unmasked sites were expressed at later stages. On the basal surfaces masked Con A sites were evident in the early stages but gradually decreased in later stages, whereas unmasked sites were relatively abundant and increased thereafter. Masked PNA sites were evident and increased very rapidly, whereas unmasked sites became observable up to the latest stage. Masked SBA sites were minimal in all three stages, and unmasked sites expressed themselves slightly at later stages. The change in composition of carbohydrates on the developing neuroectoderm was obviously different from that on the developing surface ectoderm. On the contact surface of the neural ridge, the number of masked sites of penultimate sugars was large at Con A sites, slight at PNA and SBA sites, which coexisted with unmasked sugar chain terminals in the areas where Con A sites were moderate and where PNA and SBA sites were poor. Finally, the role of masking on binding sites for Con A, PNA and SBA during neural tube closure is discussed, and the observation that the apparent masking effect on three lectin binding sites did not correspond to the content of sialic acid detected by LFA and LPA is a subject for further study.

Animals↗

PubMed1978

Microtubules, interkinetic nuclear migration and neurulation.

The hypotheses dealing with mechanisms of neurulation are reviewed briefly. The phenomenon of interkinetic nuclear migration is thought to be an important factor to be considered in the invagination of the neuroepithelium in the chick embryo. Evidence is presented that implicates cytoplasmic microtubules in this phenomenon. It is suggested that microtubules not only participate in cell elongation but also that they are involved, through interkinetic nuclear migration, in the broadening of the basal region of the cells; this widening progressively creates the strain that ensures the invagination of the neuroepithelium.

Animals↗

PubMed1992

Studies on valproate-induced perturbations of neurulation in the explanted chick embryo.

The effect of the anticonvulsant sodium valproate on in vitro neurulation of the chick embryo, explanted after a 25-h in ovo incubation period, is described. Sodium valproate, at concentrations of 0.5-1.5 mM did not appear to have any profound effect on embryo growth when assessed by light microscopy. However scanning electron microscopy revealed a dose-dependent increase in the incidence of open anterior and posterior neuropores after 20 h of in vitro development (Stage 11). Concentrations of sodium valproate which were greater than 1.5 mM markedly increased the number of gross malformations, which were manifested as a complete disruption of the neural tube along its entire length. Failure of neuropore closure could not be attributed to a drug-induced neurodevelopmental delay as these defects were still apparent following 27 h of in vitro culture, a time coincident with the onset of embryo torsion.

Animals↗