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PubMed1986

Calcium and neurulation in mammalian embryos. II. Effects of cytoskeletal inhibitors and calcium antagonists on the neural folds of rat embryos.

The role of calcium in neurulation in mammalian embryos has been studied by culturing rat embryos at 10.4 days of gestation, when the cephalic neural folds have elevated but not fused, in serum containing cytoskeletal inhibitors or calcium antagonists. The effects of these antagonists on the morphology of the cephalic neural folds have been examined by scanning electron microscopy. The different agents caused the cephalic neural folds to part to varying degrees. The neural folds were classified as intact (normal), open (folds parted up to 90 degrees with each other), flattened (folds parted from 90 degrees to 180 degrees) or collapsed (folds parted more than 180 degrees). The microtubule inhibitors colchicine and nocodazole at 10(-4) M respectively cause the cephalic neural folds of 10.4-day embryos to collapse after 60 min. At 5.2 X 10(-6)M the microfilament inhibitor cytochalasin B causes the folds to open after 60 min. Longer term culture of 9.5-day embryos for 24 h in diazepam, which is reported to inhibit myosin synthesis, causes general developmental retardation including a delay in the closure of the neural tube. Culture of 10.4-day rat embryos for 60 min in papaverine at 2.4 X 10(-4) M or gallopamil (D-600) at 5.0 X 10(-4) M, agents which reduce the entry of calcium into cells, causes opening of the elevated cephalic neural folds. In contrast TMB-8, which is purported to perturb some intracellular calcium-dependent functions, does not cause opening of the elevated cephalic neural folds, even at high concentrations. The results suggest that both microtubules and microfilaments are essential to the maintenance of the elevated cephalic neural folds in rat embryos. The results are also compatible with the idea that calcium ion flux across the membranes of the neuroepithelial cells might be important for the elevation of the neural folds, and thus for successful neurulation.

Animals↗

PubMed1986

Neurulation and the cortical tractor model for epithelial folding.

We present here a new model for epithelial morphogenesis, which we call the 'cortical tractor model'. This model assumes that the motile activities of epithelial cells are similar to those of mesenchymal cells, with the added constraint that the cells in an epithelial sheet remain attached at their apical circumference. In particular, we assert that there is a time-averaged motion of cortical cytoplasm which flows from the basal and lateral surfaces to the apical region. This cortical flow carries with it membrane and adhesive structures that are inserted basally and resorbed apically. Thus the apical seal that characterizes epithelial sheets is a dynamic structure: it is continuously created by the cortical flow which piles up components near where they are recycled in the apical region. By use of mechanical analyses and computer simulations we demonstrate that the cortical tractor motion can reproduce a variety of epithelial motions, including columnarization (placode formation), invagination and rolling. It also provides a mechanism for driving active cell rearrangements within an epithelial sheet, while maintaining the integrity of the apical seal. Active repacking of epithelial cells appears to drive a number of morphogenetic processes. Neurulation in amphibians provides an example of a process in which all four of the above morphogenetic movements appear to play a role. Here we reexamine the process of neurulation in amphibians in light of the cortical tractor model, and find that it provides an integrated view of this important morphogenetic process.

Amphibians↗

PubMed1985

Calcium and neurulation in mammalian embryos.

The role of calcium in neurulation in rat embryos has been studied. Rat embryos at 10 X 4 days of gestation, when the cephalic neural folds have elevated but not fused, have been cultured in various media, and the effects of these media on the morphology of the cephalic neural folds have been observed by scanning and transmission electron microscopy. Embryos cultured in serum containing EDTA or EGTA, or in saline without divalent cations exhibit opening, then folding back ('collapse') of the cephalic neural folds. The neural cells lose their elongated shape and become rounded. Older embryos in which the cephalic neural folds have already fused do not show collapse of the neural tube. Culture of 10 X 4-day rat embryos with elevated but unfused cephalic neural folds in calcium- and magnesium-free saline to which either calcium or magnesium has been restored shows that calcium is the divalent cation which is essential for the maintenance of the elevated neural folds. In the presence of calcium, lanthanum, which competes for calcium sites, causes opening but not collapse of the elevated cephalic neural folds. Embryos treated with trypsin show dissociation of the lateral (non-neural) ectoderm but the neural folds remain elevated. If embryos in which the cephalic neural folds have been caused to collapse are further cultured in serum the folds re-elevate, although normal neural tube morphology is not completely regained. The possible implications of these observations to the understanding of the cellular mechanisms of normal neurulation, and of neural tube malformations are discussed.

Animals↗

PubMedDate not supplied

[Spatial-temporal patterns of the cell cycles in embryos of the clawed toad during gastrulation and neurulation].

The dynamics of DNA synthesis and duration of G2-phases in different dorso-ventral zones and cell layers were studied using 3H-thymidine in the X. laevis embryos during gastrulation and neurulation. Gradients of the index of labelled nuclei and of the rate of 3H-thymidine incorporation decreasing in the ventro-dorsal direction were observed during the whole period of gastrulation. In the end of gastrulation a wave of increase of the index of labelled nuclei and of the rate of 3H-thymidine incorporation proceeds in the same direction and, as a result, both the gradients are inverted. A high positive correlation was found between the simultaneously registered indices of labelled nuclei in different cell layers of the same dorso-ventral zones. The data were obtained suggesting the ventro-dorsal migration of cells in G2-phase. A conclusion is drawn that the regulation of cell cycles during gastrulation--neurulation obeys integral laws among which the waves of cell entrance in S-phase play an important role.

Animals↗

PubMed1984

Generation of anencephaly: 1. Aberrant neurulation and 2. Conversion of exencephaly to anencephaly.

An experimental model for anencephaly was used to focus on two important aspects of the development of anencephaly: neurulation and conversion of exencephaly to anencephaly. Vitamin A was administered to pregnant rats on gestational days nine and ten. The animals were killed on successive gestational days to allow study of the development of anencephaly. The scanning electron microscope revealed filopodia and lamellopodia as the predominant mode of initial neural fold contact in the controls. Intertwining and overlapping of filopodia and lamellopodia with fusion of the adjacent cutaneous ectoderm completed neurulation. In embryos developing anencephaly, filopodia and lamellopodia never made contact above the cervical region and exencephaly resulted. The first evidence of the conversion of exencephaly to anencephaly was profound, labyrinthine expansion of the extracellular space of the telencephalic mantle. In spite of normal vascular patency and intact vessel walls, the exencephalic malformation spontaneously disintegrated, converting the lesion to anencephaly. The causes for tissue disintegration other than infarction must be considered in reconstructing the pathogenesis of anencephaly.

Anencephaly↗

PubMed1982

Culture of rat embryos with beta-D-xyloside: evidence of a role for proteoglycans in neurulation.

Day 9 rat embryos were cultured during the period of cranial neurulation in medium containing 1 mm beta-d-xyloside, a substance which inhibits proteoglycan synthesis while stimulating the synthesis of free chains of chondroitin sulphate. The purpose of this investigation was to elucidate the morphogenetic role of chondroitin sulphate, a component of the neuroepithelial basement membrane and other extracellular regions, and to discover whether it was present in the form of proteoglycan. The histochemical results indicated a great reduction in chondroitin/chondroitin sulphate and in heparan sulphate in the neuroepithelial basement membrane and elsewhere, in beta-D-xyloside-cultured embryos. Ultrastructural studies showed an effect on the structural integrity of the neuroepithelium, with breaks in the basement membrane and abnormal form of apical microfilament bundles. These observations were correlated morphogenetically with failure of the convex neural folds to be converted to flat-concave structures, and to change their epithelial organization from columnar to pseudostratified. Neural crest cell migration was slightly retarded but apparently normal. The results are interpreted as indicating that the sulphated glycosaminoglycans, chondroitin/chondroitin sulphate and heparan sulphate, are present in the form of proteoglycan in the neuroepithelial basement membrane and elsewhere in the cranial region of day 9/day 10 rat embryos, and that they have a morphogenetic function during cranial neurulation.

Animals↗

PubMedDate not supplied

[Mitotic activity of the embryonic tissues of the clawed toad in the period of gastrulation and neurulation].

The mitotic indices (MI) were measured on serial transverse sections in ecto- and mesoderm of different dorsoventral zones of the X. laevis embryos from the late blastula stage till the end of neurulation. The MI were shown to fall simultaneously in mesoderm of all zones during the transition from middle to late gastrula (stages 12 and 13) and in ectoderm of all zones at the late gastrula stage (12 1/2 and 13) and rise synchronously in the dorsal and lateral ectoderm and lateral mesoderm during neurulation. In the most cases the rise of MI coincided with the periods of active morphogenetic movements of the given area and the fall of MI with the cessation of these movements.

Animals↗

PubMed1993

The effects of periconceptional folic acid and vitamin supplementation on maternal folate levels and on neurulating hamster embryos in vivo.

We studied the effects of periconceptional oral supplementation of folic acid and vitamins on the maternal red blood cell (RBC) folate level of golden hamsters (Mesocricetus auratus, Waterhouse). The effects of folate deficiency and supplementation on the process of neurulation and the incidence of resorptions were evaluated. Groups of at least eleven mature virgin female hamsters were placed on one of six specific regimens which started two weeks prior to mating and continued until sacrifice on day nine of pregnancy. Just prior to sacrifice, blood samples were drawn by cardiac puncture to measure maternal folic acid levels in red blood cells. The staging of the embryos was based on O'Rahill's modification of Streeter's developmental horizons in human embryos. Considerable variation was observed in the stage of embryonic development of 9-day-old hamster embryos, both between littermates and between litters of the same gestational age. A high overall incidence of open neural tubes was observed, which did not reflect neural tube closure failures. A folate-free diet caused retardation of the embryonic development, although maternal folate levels were unaffected (p < 0.01). The RBC folate levels in the animals which received oral supplementation with folic acid was significantly higher than that in the unsupplemented controls (p < 0.001). Folic acid supplementation alone increased the RBC folate level significantly more than combined supplementation with multivitamins (p < 0.001). The data indicate that oral supplementation with folic acid and/or multivitamins produce adequate maternal RBC folate levels. An inadequate maternal folate intake can affect the growth of neurulating embryos even if the maternal RBC folate levels are still sufficient.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed2005

Strychnine induces embryotoxicity in rat neurulation.

Administering strychnine, a potent antagonist of glycine receptors, to pregnant rats caused marked toxic effects on the ensuing embryos. The embryotoxic effects of strychnine were compared with those induced by retinal palmitate during rat neurulation; and it was found that strychnine was stronger than retinal palmitate in a number of abnormalities such as anencephaly, general aplasy and abnormal cerebral vesicles. Although the glycine receptor beta1 subunit mRNA was found to be expressed in the embryos when strychnine was administered to the mother rats, its presence may not fully account for the toxic effects and it may be that strychnine is targeting also other molecules, such as the nicotinic receptor that has been found early in development.

Animals↗

PubMed1998

Neurulation abnormalities secondary to altered gene expression in neural tube defect susceptible Splotch embryos.

The murine mutant Splotch (Sp) is a well-established model for studying neural tube closure defects. In the current investigation, the progression through neural tube closure (NTC) as well as the expression patterns of 12 developmentally regulated genes were examined in the neural tissue of wildtype (+/+), Splotch heterozygous (Sp/+), and Splotch homozygous (Sp/Sp) embryos during neurulation. The overall growth of the embryos, as measured by the number of somite pairs, did not differ significantly between the three genotypes at any of the collection time-points. There was, however, a significant delay in the progression through NTC for both the Sp/+ and Sp/Sp embryos. A univariate analysis on the expression of the 12 candidate genes (bcl-2, FBP-2, Hmx-2, Msx-3, N-cam, N-cad, noggin, p53, Pax-3, Shh, Wee-1, wnt-1) revealed that although 11 were statistically altered, across time or by genotype, there were no significant interactions between gestation age and genotype for any of these genes during NTC. However, a multivariate statistical analysis on the simultaneous expression of these genes revealed interactions at both gestation day (GD) 8:12 (day:hour) and 9:00 among Pax-3, N-cam, N-cad, bcl-2, p53, and Wee-1 that could potentially explain the aberrant NTC. The data from these studies suggest that a disruption in the genes that govern the cell cycle or extracellular matrices of the developing neural tube might play a critical role in the occurrence of the NTDs observed in Splotch embryos.

Animals↗

PubMedDate not supplied

Gene delivery to the neurulating embryo during culture.

Modulating expression of specific genes during embryogenesis will help elucidate their role in development. Transient overexpression of specific genes can be accomplished by adding additional copies, or else antisense transcripts can be used to block expression. Manipulation of gene expression requires an efficient, nontoxic gene delivery system. We compared a plasmid and a replication-defective adenovirus (Ad5) as methods of delivering genes to the embryo during the neurulation stage of development. Both vectors utilized a construct containing the bacterial beta-galactosidase reporter gene under the control of the human cytomegalovirus early gene promoter and the SV40 polyadenylation signal. Vectors were delivered by intraamniotic microinjection to embryos prepared for whole-embryo culture. Plasmid transfection experiments were done with and without polycationic lipid (lipofectamine, 20 or 125 micrograms/microliter) enhancement at 0.1 and 0.01 microgram per embryo. Twenty-six hours after transfection with plasmid only, embryos appeared normal, but had very weak gene expression which was detected only after extended periods of staining. In contrast, adenovirus gene delivery was successful. While high concentrations of virus (6 x 10(8) particles/ microliter) elicited significant malformations, lower concentrations (1.5 x 10(8) particles/microliter) produced no malformations and intense gene expression. Time-course studies revealed staining at 6 hr postinjection, and intense staining at 26 hr. Staining appeared primarily in the neurectoderm and cells derived from the neurectoderm. This pattern of gene expression was confirmed using a green fluorescent protein-expressing adenovirus. Rapid induction of gene expression with no toxicity is critical to the utility of this technique within the whole-embryo culture system. Clearly, Ad5 transduction provides a more useful tool than plasmid vectors.

Adenoviridae↗

PubMed1996

Expression of neurotrophin trk and p75 receptors in quail embryos undergoing gastrulation and neurulation.

We have previously demonstrated the presence of mRNA for the full-length neurotrophin receptors trkA, trkB and trkC in quail embryos from stages 1 through 6 using reverse transcription followed by the polymerase chain reaction (RT-PCR; Yao et al. [1994] Dev. Biol. 165: 727-730). Furthermore, we showed that mRNA for the neurotrophins brain-derived neurotrophic factor and neurotrophin-3 was present from stage 1 onward, while nerve growth factor mRNA began to be expressed at stage 5. In the present study, wholemount in situ hybridization was used to localize full-length trk mRNA in embryos from stages 3 through 10. Structures expressing trkC mRNA included the primitive streak and Hensen's node, the neural plate or notochord, somites and the rostral neural tube. trkA and trkB mRNA were expressed at much lower levels than trkC mRNA; however, staining was detected on the primitive streak and Hensen's node. In addition to trk mRNA, we have also demonstrated the presence of full-length Trk protein in embryos from stages 3 through 11, suggesting that the trk mRNA detected at these early stages is translated into functional cell surface receptors. To support this hypothesis, we have shown that neurotrophins can induce phosphorylation of Trk on tyrosine residues, at least at stage 11. We also detected mRNA and protein for the nontyrosine kinase neurotrophin receptor, p75, at similar stages. The presence of neurotrophin receptors, as well as neurotrophin mRNA, in embryos undergoing gastrulation and neurulation leads to speculation that neurotrophins may be playing a role in these processes.

Animals↗

PubMed1998

G1-phase regulators, cyclin D1, cyclin D2, and cyclin D3: up-regulation at gastrulation and dynamic expression during neurulation.

Gastrulation in rodents is associated with an increase in the rate of growth and with the start of differentiation within the embryo proper. In an effort to understand the role played by the cell cycle control in these processes, expression of cyclin D1, D2, and D3--three major positive regulators of the G1/S transition--has been investigated by in situ hybrization and RT-PCR. Cyclin D1 and D2 transcripts are first detected in the epiblast at gastrulation, when a proliferative burst occurs, and subsequently in its differentiated derivatives within the embryo proper, indicating that activation of their expression takes place prior to the differentiation of epiblast progenitors. In contrast, cyclin D3 transcript is undetectable in the epiblast itself and its expression is activated exclusively in extraembryonic tissues of both epiblast and trophoblast origin. During neurulation, expression of each cyclin D RNA is dynamically regulated along the anterior-posterior axis. In the hindbrain, cyclin D1 and D2 show distinct segment-specific restricted expression and this pattern is conserved between mouse and chick. These results strongly suggest that D-type cyclins act as developmental regulators.

Animals↗

PubMed1994

Neurulation in the normal human embryo.

The neural groove and folds are first seen during stage 8 (about 18 postovulatory days). Two days later (stage 9) the three main divisions of the brain, which are not cerebral vesicles, can be distinguished while the neural groove is still completely open. Two days later (stage 10) the neural folds begin to fuse near the junction between brain and spinal cord, when neural crest cells are arising mainly from the neural ectoderm. The rostral (or cephalic) neuropore closes within a few hours during stage 11 (about 24 days). The closure is bidirectional; it takes place from the dorsal and terminal lips and may occur in several areas simultaneously. The two lips, however, behave differently. The caudal neuropore takes a day to close during stage 12 (about 26 days) and the level of final closure is approximately at future somitic pair 31, which corresponds to the level of sacral vertebra 2. At stage 13 (4 weeks) the neural tube is normally completely closed. Secondary neurulation, which begins at stage 12, is the differentiation of the caudal part of the neural tube from the caudal eminence (or end-bud) without the intermediate phase of a neural plate.

Embryonic and Fetal Development↗

PubMed1994

Molecular genetics of neurulation.

The formation of the neural tube begins during gastrulation when ectoderm, an epithelial sheet on the outside of the embryo, is induced to form the neural plate. During the process of neural induction, the epithelium of the neural plate is regionalized along both the dorsoventral and anteroposterior axes of the embryo; this regionalization is likely to contribute to the cellular processes underlying neurulation. Genes whose expression marks the formation and regionalization of the neural plate and which encode cell adhesion molecules or putative transcription factors have been recently identified. The differential expression of these genes apparently subdivides the epithelium of the neural plate into small regions. Evidence from transgenic embryo experiments supports the idea that the differential expression of these genes in the neural plate plays a role in neural tube formation.

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↗