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PubMed1992

Valproic acid induced abnormal development of the central nervous system of three species of amphibians: implications for neural tube defects and alternative experimental systems.

Embryos of Ambystoma mexicanum, Xenopus laevis, and Hyperolius viridiflavus taeniatus were exposed to various concentrations of valproic acid (VPA: 0.1, 1.5, 10 mM) from blastula stage (S) 9 on up to advanced gastrulation of control embryos (S 11 1/2-12). At 10 and 5 mM VPA early development was affected in all species tested. However, the most pronounced effects occurred in Ambystoma: the neural folds appeared delayed and showed a flattened and wavy shape; the neural tube was not formed and embryos successively died. In Xenopus and Hyperolius (10, 5 mM VPA) the beginning of gastrulation was delayed up to neurulation of control embryos. In Xenopus many of the embryos completed neurulation, whereas some embryos exposed to 10 mM VPA showed neural tube defects (NTDs) of different type and degree (open neural tube at different regions of the dorsum). In Hyperolius neural folds arose around the blastoporus and fused later on (earlier in embryos treated with 5 mM VPA), but the shape of these embryos was abnormal and the development was not continued (pronounced effect at 10 mM VPA). Comparing the three species, Xenopus proved to be the least sensitive species (at 5 mM VPA 14.2% NTDs of total malformations compared to 100% in the other species). The most sensitive species, Ambystoma, developed head-oedema at 1 mM VPA, whereas the anurans were not affected. Our results suggest a similar mechanism of VPA-induced NTDs in mammals and amphibians.

Abnormalities, Drug-Induced↗

PubMed1988

A comparative study of the effects of retinoic acid given during the critical period for inducing spina bifida in mice and hamsters.

Spina bifida occurred in the offspring of golden Syrian hamsters treated on day 8 of gestation, and CD-1 mice treated on day 9, with 80 mg/kg of retinoic acid. Light microscopic examination of term fetuses demonstrated that myeloschisis was the characteristic form of the defect in mice, whereas myelocystocele was the predominant type of spina bifida induced in the hamster. To investigate the pathogenesis of these defects, a comparative study was undertaken by light microscopy and scanning electron microscopy of the changes occurring in caudal embryonic tissues during the initial 48 hr following maternal treatment. Within 18 hr of exposure, similar effects were observed in both species. These included distortion of the neural folds at the level of the posterior neuropore, vascular damage and hematoma formation, malformation of the notochord, and abnormalities of secondary neurulation. No differences were observed that we thought could account for the apparent variation in the pattern of malformations seen in the term litters. Rather, the dissimilarity may reflect species differences in the position of the posterior neuropore in the neuraxis and in the extent to which secondary neurulation contributes to the development of the lumbosacral cord segments.

Animals↗

PubMed1990

Phenylalanine and its metabolites induce embryopathies in mouse embryos in culture.

The aim of this study was to determine the teratogenicity of phenylalanine (Phe) and Phe metabolites in neurulating mouse embryos. Therefore, the system of whole embryo culture was employed and D9 (neurulating) mouse embryos were exposed to Phe, phenylethylamine (PEA), phenylpyruvic acid (PPA), phenylacetic acid (PAA), 2-OH phenylacetic acid (2-OH PAA), and phenyl-lactic acid (PLA) at concentrations ranging from 0.01 mM to 10 mM for 24 hours. After 24 hours, embryos were examined for morphological abnormalities and protein content by the Lowry method. Phe at 1 and 6 mM concentrations was not teratogenic; however, 10 mM inhibited cranial neural tube closure in 82% of the embryos. PEA was the most toxic factor and concentrations of 1 and 10 mM were embryo-lethal, whereas neural tube closure defects (NTDs) were observed in 67% of the embryos at 0.1 mM. 2-OH PAA was the second most toxic metabolite with concentrations of 1 and 10 mM producing NTDs in 10 and 100% of the embryos, respectively. PLA and PAA produced no NTDs at concentrations of 1 mM, 60% at 5 mM, and 100% at 10 mM. Finally, PPA produced approximately 50% NTDs at both 1 mM and 10 mM concentrations. PLA, PAA, 2-OH PAA, and PPA produced a significant reduction in embryonic protein, and PEA and 2-OH PAA reduced yolk sac protein values. PEA, 2-OH PAA, PPA, PAA, and PLA also produced craniofacial abnormalities, i.e., incomplete expansion of the forebrain, collapse of the optic vesicle, and hypoplasia of the mandible and/or the maxilla.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Embryotoxic effects of chlorobutanol in cultured mouse embryos.

Chlorobutanol (CB) is a commonly used preservative which is added to numerous pharmaceutical preparations, and it is the active ingredient in certain oral sedatives and topical anesthetics. Chlorobutanol has demonstrated adverse effects in adult tissues, but CB has not been previously investigated for its effect on the developing whole embryo. The method of whole-embryo culture was used in this study to expose mouse embryos during two stages of organogenesis to CB at final concentrations of 0 (control), 10, 25, 50, 100, and 200 micrograms/ml. Embryos were evaluated for heart rate (HR), malformations, and somite number, and embryos and visceral yolk sacs (VYSs) were assayed for total protein content as a measure of overall growth. Neurulating (3-6 somite) embryos were malformed and growth retarded by exposure to CB concentrations > or = 25 micrograms/ml, with decreased VYS growth at > or = 50 micrograms/ml and decreased HR at > or = 100 micrograms/ml CB. Early limb-bud stage (20-25 somite) embryos were malformed at CB concentrations > or = 50 micrograms/ml and growth retarded at > or = 100 micrograms/ml, with decreased VYS growth at 200 micrograms/ml and decreased HR at > or = 100 micrograms/ml CB. Thus, CB produces dysmorphogenesis in mouse embryos in vitro, and neurulating embryos are somewhat less sensitive than early limb-bud stage embryos. The concentrations of CB that interfere with normal embryonic development are within the range of human blood levels measured following multiple doses of CB. Preparations containing CB should be used with caution during pregnancy, particularly when repeated dosing may allow accumulation of CB to potentially embryotoxic levels.

Abnormalities, Drug-Induced↗

PubMed1994

Volume and glucose concentration of rat amniotic fluid: effects on embryo nutrition and axis rotation.

In order to pursue our previous studies of the changes in neural tube microvilli produced by glucose, we developed a micro method of measuring glucose concentration in the very small volumes of amniotic fluid during neurulation. The volume of amniotic fluid was found to increase nearly 10-fold during major neurulation (day 10 to day 11 in the rat). This increase in volume and our repeated observations that physical removal of the restraining amnion initiates embryonic rotation leads us to propose that the growth of the amniotic cavity is essential for conversion from the ventral- to dorsi-flexion of the embryonic axis. Amniotic fluid volume continues to increase until day 18 but dropped by day 20. A method for glucose determination was developed using the color reaction on glucose oxidase indicator paper. The intensity of the color was analyzed with a color scanner. Amniotic glucose was 27.1 +/- 1.6 mg/dl on day 10 and continued in this range with some fluctuation until day 20 when it decreased. We isolated days 10, 11, and 16 embryonic sites from their decidua and incubated them at 0 degrees C and 38 degrees C while measuring glucose concentration. The glucose concentration did not show significant decrease at 0 degrees C on day 10 or 11 or on day 16 at 38 degrees C. At 38 degrees C the day 10 embryo amniotic fluid glucose disappeared after 22 minutes and the day 11 amniotic fluid glucose was gone in 34 minutes. These depletion times were statistically different. The magnitude of glucose depletion on day 10 was shown by calculation to be approximately 323 mumoles/gm protein per hour which is a substantial portion of the glucose utilized by the embryo as determined in previous experiments (731 mumoles/gm protein per hour). This model may serve as a way to study glucose utilization by embryos after their exposure to various teratogens.

Amniotic Fluid↗

PubMed1997

Developmental defects in mouse embryos lacking N-cadherin.

To investigate the functions of N-cadherin in vivo, we have mutated the gene encoding this adhesion protein in mice. Although N-cadherin is expressed at the time of gastrulation and neurulation, both neurulation and somitogenesis initiate apparently normally in homozygous mutant embryos. However, the resulting structures are often malformed. The somites of the mutant embryos are small, irregularly shaped, and less cohesive compared with those of their wild-type littermates, and the epithelial organization of the somites is partially disrupted. Undulation of the neural tube is also observed in the mutant embryos. Homozygous mutant embryos die by Day 10 of gestation. The mesodermal and endodermal cell layers of the yolk sac are separated in the mutants. The most dramatic cell adhesion defect is observed in the primitive heart; although myocardial tissue forms initially, the myocytes subsequently dissociate and the heart tube fails to develop normally. In vitro studies of cardiac myocytes derived from N-cadherin mutant embryos show that the cells can loosely aggregate and beat synchronously, demonstrating that electrical coupling can occur between N-cadherin-deficient cardiac myocytes. These results show that N-cadherin plays a critical role in early heart development as well as in other morphogenetic processes.

Animals↗

PubMed1997

Epithelial cell wedging and neural trough formation are induced planarly in Xenopus, without persistent vertical interactions with mesoderm.

In this study we investigate the induction of the cell behaviors underlying neurulation in the frog, Xenopus laevis. Although planar signals from the organizer can induce convergent extension movements of the posterior neural tissue in explants, the remaining morphogenic processes of neurulation do not appear to occur in absence of vertical interactions with the organizer (R. Keller et al. , 1992, Dev. Dyn. 193, 218-234). These processes include: (1) cell elongation perpendicular to the plane of the epithelium, forming the neural plate; (2) cell wedging, which rolls the neural plate into a trough; (3) intercalation of two layers of neural plate cells to form one layer; and (4) fusion of the neural folds. To allow planar signaling between all the inducing tissues of the involuting marginal zone and the responding prospective ectoderm, we have designed a "giant sandwich" explant. In these explants, cell elongation and wedging are induced in the superficial neural layer by planar signals without persistent vertical interactions with underlying, involuted mesoderm. A neural trough forms, and neural folds form and approach one another. However, the neural folds do not fuse with one another, and the deep cells of these explants do not undergo their normal behaviors of elongation, wedging, and intercalation between the superficial neural cells, even when planar signals are supplemented with vertical signaling until the late midgastrula (stage 11.5). Vertical interactions with mesoderm during and beyond the late gastrula stage were required for expression of these deep cell behaviors and for neural fold fusion. These explants offer a way to regulate deep and superficial cell behaviors and thus make possible the analysis of the relative roles of these behaviors in closing the neural tube.

Animals↗

PubMed1999

Time course of ion channel development in Xenopus muscle induced in vitro by activin.

During the process of mesoderm specification in Xenopus embryos, cells of the equatorial region are induced to form mesoderm in response to signals from the underlying endodermal cells. One mesodermal cell type resulting from this in vivo induction is skeletal muscle, which has a very specific and tightly regulated course of electrical and morphological development. Previously, electrical development could be analyzed only after neurulation, once myocytes could be morphologically identified. In vitro, activin triggers a cascade of events leading to the development of specific mesodermal tissues, including skeletal muscle; however, the precise role of activin in vivo is less clear. Much is now known about the mechanism and control of activin action, but very little is known about the subsequent time course of differentiation of activin-induced muscle. Such muscle is routinely identified by the presence of a small number of specific markers which, although they accurately confirm the presence of muscle, give little indication of the time course or quantitative aspects of muscle development. One of the most important functional aspects of muscle development is the acquisition of the complex electrical properties which allow it to function normally. Here we assess the ability of activin to drive in vitro the normal highly regulated sequence of electrical development in skeletal muscle. We find that in most, but not all, respects the normal time course of development of voltage-gated ion currents is well reproduced in activin-induced muscle. This characterization strengthens the case for activin as an agent capable of inducing the detailed developmental program of muscle and now allows for analysis of the regulation of electrical development prior to neurulation.

Activins↗

PubMed1999

Ventral cell rearrangements contribute to anterior-posterior axis lengthening between neurula and tailbud stages in Xenopus laevis.

Studies of morphogenesis in early Xenopus embryos have focused primarily on gastrulation and neurulation. Immediately following these stages is another period of intense morphogenetic activity, the neurula-to-tailbud transition. During this period the embryo is transformed from the spherical shape of the early stages into the long, thin shape of the tailbud stages. While gastrulation and neurulation depend largely on active cell rearrangement and cell shape changes in dorsal tissues, we find that the neurula-to-tailbud transition depends in part on activities of ventral cells. Ventral explants of neurula lengthen autonomously as much as the ventral sides of intact embryos, while dorsal explants lengthen less than the dorsal sides of intact embryos. Analyses of cell division, cell shapes, and cell rearrangement by transplantation of labeled cells and by time lapse recordings in live intact embryos concur that cell rearrangements in ventral mesoderm and ectoderm contribute to the autonomous anterior-posterior axis lengthening of ventral explants between neurula and tailbud stages.

Animals↗

PubMed2000

Primary neuronal differentiation in Xenopus embryos is linked to the beta(3) subunit of the sodium pump.

In amphibian embryos, activation of additional sodium pumps in neural plate cell membranes ensures that neural plate-derived neurons differentiate subsequently in the neural tube. When the sodium pump is inhibited during the mid-neural fold stages, neuronal differentiation fails. The effect is irreversible. We find that these events operate through the Na pump beta(3) subunit. When neural plate-specific Na pumps are activated, transcripts for beta(3) decline precipitately during the mid-neural fold stages, first in the neural plate and then in the dorsal mesoderm. As the neural tube closes, beta(3) returns, specifically in motor neurons and interneurons. Inhibition of the Na pump with the cardiac glycoside strophanthidin prevents the normal fall in beta(3) during neurulation: beta(3) is maintained in the neural plate until the neural tube closes, but lost from the dorsal mesoderm. Complete elimination of beta(3) transcripts from dorsal structures then occurs. Inhibiting the Na pump does not induce cell death (assessed by TUNEL staining) in the nervous system. Transcripts for X-Delta, NeuroD, and GSK3beta are not affected by inhibition of the Na pump. Xotch and N-tubulin transcripts fall to very low levels and Xotch disappears permanently from the nervous system. When beta(3) transcript expression is maintained throughout neurulation, by over expression of injected mRNAs, Xotch is eliminated from the neural tube and somites and switches to the ectoderm.

Animals↗

PubMed2000

Relationship between gene expression domains of Xsnail, Xslug, and Xtwist and cell movement in the prospective neural crest of Xenopus.

The markers Xslug, Xsnail, and Xtwist all are expressed in the presumptive neural folds and are thought to delineate the presumptive neural crest. However, their interrelationship and relative spatiotemporal distributions are not well understood. Here, we present a detailed in situ hybridization analysis of the relative patterns of expression of these transcription factors from gastrulation through neurulation and post-neural crest migration. The three genes mark the prospective neural crest and roof plate, coming on sequentially, with Xsnail preceding Xslug preceding Xtwist. By combining gene expression analysis with a fate map of the same region using DiI labeling, we determined the correspondence between early and late domains of gene expression. At the beginning of gastrulation, Xsnail is present in a unique domain of expression in a lateral region of the embryo in both superficial and deep layers of the ectoderm, as are Xslug and Xtwist. During gastrulation and neurulation, the superficial layer moves faster toward the dorsal midline than the deep layer, producing a relative shift in these cell populations. By early neurula stage, the Xsnail domain is split into a medial domain in the superficial ectoderm (fated to become the roof plate) and a lateral domain in the deep layer of the ectoderm (fated to become neural crest). Xsnail is down-regulated in the most anterior neural plate and up-regulated in the posterior neural plate. Our results show that changes in the expression of Xsnail, Xslug, and Xtwist are a consequence of active cell movement in some regions coupled with dynamic changes in gene expression in other regions.

Animals↗

PubMed2000

Retinoid signaling is required to complete the vertebrate cardiac left/right asymmetry pathway.

Vitamin A-deficient (VAD) quail embryos have severe abnormalities, including a high incidence of reversed cardiac situs. Using this model we examined in vivo the physiological function of vitamin A in the left/right (L/R) cardiac asymmetry pathway. Molecular analysis reveals the expression of early asymmetry genes activin receptor IIa, sonic hedgehog, Caronte, Lefty-1, and Fgf8 to be unaffected by the lack of retinoids, while expression of the downstream genes nodal-related, snail-related (cSnR), and Pitx2 is altered. In VAD embryos nodal expression in left lateral plate mesoderm (LPM) is severely downregulated and the expression domain altered during neurulation. Similarly, the expression of cSnR in the right LPM and of Pitx2 in the left side posterior heart-forming region (HFR) is downregulated in the VAD embryos. The lack of retinoids does not cause randomization or ectopic expression of nodal, cSnR, or Pitx2. At the six- to eight-somite stage nodal is expressed transiently in the left posterior HFR of normal quail embryos; this expression is missing in VAD embryos and may be linked to the loss of Pitx2 expression in this region of VAD quail embryos. Administration of retinoids to VAD embryos prior to the six-somite stage rescues the expression of nodal, cSnR, and Pitx2 as well as the randomized VAD cardiac phenotype. There is an absolute requirement for retinoids at the four- to five-somite developmental window for cardiogenesis and cardiac L/R specification to proceed normally. We conclude that retinoids do not regulate the left/right-specific sidedness assignments for expression of genes on the vertebrate cardiac asymmetry pathway, but are required during neurulation for the maintenance of adequate levels of their expression and for the development of the posterior heart tube and a loopable heart. Cardiac asymmetry may be but one of several critical events regulated by retinoid signaling in the retinoid-sensitive developmental window.

Activin Receptors, Type II↗

PubMed1995

Xenopus F-cadherin, a novel member of the cadherin family of cell adhesion molecules, is expressed at boundaries in the neural tube.

Development of the vertebrate CNS begins during neurulation when the neural plate gives rise to the neural tube. During neurulation, the different regions of the CNS can be identified in part by the appearance of flexures in the walls of the neural tube. Here we report the isolation and characterization of F-cadherin; a novel member of the cadherin family of cell adhesion molecules, which is expressed at flexures in the neural tube of Xenopus embryos. We show that F-cadherin is first expressed at neural plate stages, that its expression is altered when patterning of the neural tube is perturbed, and that its expression marks boundaries in the neural tube where cell mixing is restricted. These observations suggest that F-cadherin contributes to the regionalization of the neural tube perhaps by mediating differential cell adhesion.

Amino Acid Sequence↗

PubMed1997

A role of midkine in the development of the neuromuscular junction.

Midkine (MK) is a member of a family of developmentally regulated neurotrophic and heparin-binding growth factors. It is expressed during the midgestation period in a retinoid-acid dependent manner during embryogenesis in the mouse. In vitro, it promotes neurite outgrowth from spinal cord neurons and cell migration. It expression is strongest in the central nervous system, thus suggesting a function for this protein in neural development. In this study, the role of MK in synaptogenesis was examined in the Xenopus system. A Xenopus MK cDNA was cloned from an embryonic library encompassing neurulation and synaptogenesis stages. By Northern blot analysis, MK mRNA was detected from the onset of neurulation and throughout the stages of synaptogenesis in the Xenopus embryo. This suggests that MK is also an important growth regulator in Xenopus embryogenesis. To study the function of MK in the development of the neuromuscular junction (NMJ), fusion proteins were made and their ability to induce the formation of acetylcholine receptor (AChR) clusters in cultured muscle cells was studied. Beads coated with MK strongly induce AChR clustering. When nerve-muscle cocultures were labeled with antibodies made against the MK fusion protein, MK immunoreactivity was detected at the NMJ. Unlike heparin-binding growth-associated molecule (HB-GAM), another member of this growth factor family, MK expression cannot be detected in the muscle but is present in spinal cord neurites. Consistent with these in vitro data is the observation that MK mRNA is only localized in the central nervous system but the protein is deposited at the intersomitic junction where the NMJ is located in vivo. Exogenously applied MK does bind to the heparan sulfate proteoglycan on the surface of Xenopus muscle cells. Agrin, a heparan-sulfate proteoglycan that induces the formation of AChR clusters in cultured muscle cells, binds strongly to MK. Bath application of MK in conjunction with agrin results in a change in the pattern of AChR clustering induced by agrin alone. These data suggest that MK is a neuron-derived factor that participates in the signal transduction process during NMJ development.

Agrin↗

PubMed1992

The vertebrate tail bud: three germ layers from one tissue.

The tail bud of amniote embryos comprises a mass of apparently undifferentiated mesenchymal cells located at the caudal limit of the embryo, representing the remains of Hensen's node and the primitive streak. These cells have the potential to give rise to a variety of different tissues including the posterior or 'secondary' neural tube, the tail gut, and somites and their derivatives. This seemingly homogeneous accumulation of cells therefore has the capacity to differentiate into tissues which in more cranial regions of the embryo are derived from cells of different germ layers. In this review, the tissue contributions of the tail bud in various vertebrate classes are discussed, with particular attention to the mesenchymal-to-epithelial transformation that characterizes the process of secondary neurulation, and which distinguishes it from the epithelial folding that occurs during primary neurulation in more cranial regions. Recent studies suggest that the transformation is accompanied by extensive changes in the cell surface oligosaccharide complement of the differentiating cells, and that the sialyted form of N-CAM is expressed both temporally and spatially in a manner that suggests a role for it in the process. The pluripotential nature of the tail bud mesenchyme may be revealed experimentally by grafting the tissue ectopically, or by culturing it on different substrata. In the latter case, the mesenchyme can be demonstrated to give rise to myocytes, chondrocytes, neuroepithelium and neural crest derivatives such as melanocytes, depending on the nature of the culture substratum. It is concluded that the tail bud mesenchyme represents a developing system which is readily amenable to experimentation and should provide insights into the general mechanisms of cell differentiation and transformation.

Amphibians↗

PubMed1988

The development of the human brain from a closed neural tube at stage 13.

Twenty-five embryos of stage 13 (28 days) were studied in detail and graphic reconstructions of seven of them were prepared. Thirty or more somitic pairs are present, and the maximum is possibly 39. The notochord is almost entirely separated from the neural tube and the alimentary epithelium, and its rostral tip is closely related to the adenohypophysial pocket. Caudal to the cloacal membrane, the caudal eminence is the site of secondary neurulation. The eminence, which usually contains isolated somites, is the area where new notochord, hindgut, and neural tube are forming. The neural cord develops into neural tube without the intermediate phase of a neural plate (secondary neurulation). Canalization is regular and the lumen is continuous with the central canal. The neural tube is now a closed system, filled with what may be termed "ependymal fluid." The brain is widening in a dorsoventral direction. Neuromeres are still detectable. The following features are distinguishable: infundibular area of D2, chiasmatic plate of D1, "adult" lamina terminalis, and commissural plate (at levels of nasal plates). The beginning of the synencephalon of D2 can be discerned. The retinal and lens discs are being defined. The mesencephalic flexure continues to diminish. The midbrain possesses a sulcus limitans, and the tegmentum may show the medial longitudinal fasciculus. The isthmic segment is clearly separated from rhombomere 1. Lateral and ventral longitudinal fasciculi are usually present in the hindbrain, and the common afferent tract is beginning. Somatic and visceral efferent fibres are seen in certain nerves: 6, 12; 5, 7, 9-11. The first indication of the cerebellum may be visible in the alar lamina of rhombomere 1. The terminal-vomeronasal crest appears. Various cranial ganglia (e.g., vestibular, superior ganglia of 9, 10) are forming. The trigeminal ganglion may show its three major divisions. Epipharyngeal placodes of pharyngeal arches 2 to 5 contribute to cranial ganglia 7, 9, and 10. The spinal neural crest is becoming segregated, and the spinal ganglia are in series with the somites. Ventral spinal roots are beginning to develop.

Brain↗

PubMed1988

Changes in peanut lectin binding sites on the neuroectoderm during neural tube formation in the bantam chick embryo.

Cell surface carbohydrates in the neurulating ectoderm of bantam chick embryos of stage 6-11 were examined using the fluorescein isothiocyanate-labeled and ferritin-labeled peanut lectin, Arachis hypogaea agglutinin (PNA), which is Gal beta 1----3GalNAc specific. Weak fluorescence showing PNA binding sites was seen on the apical surfaces of neural plate cells. On the surfaces of neural tube cells the fluorescence was more intense and appeared as a band. When using ferritin particles as a quantitative EM marker, only a few PNA binding sites covering the apical surfaces of the basal plate cells during the neural plate stage were seen (274.3 +/- 18.67 ferritin particles/micron 2). As neural tube formation advanced, the number of the ferritin labeled PNA binding sites increased as was to be expected from the fluorescent label experiment. At the neural ridge contact stage there were 2.5 times more binding sites than at the neural plate stage. After this period, the lectin binding sites showed no significant changes. These results were the inverse of those for RCAI or WGA lectins previously reported by us. These observations suggest that sugar residues or the sugar-chain skeletons on the neuroectoderm are altered during neurulation.

Animals↗

PubMed1986

Binding pattern of ferritin-labeled lectins (RCAI and WGA) during neural tube closure in the bantam embryo.

Cell surface sugar residues in neurulating ectoderms of bantam chick embryos of stage 4-11 were examined using ferritin-labeled Ricinus communis (RCAI) and Wheat germ agglutinin (WGA). RCAI binding sites densely covered the apical surfaces of the basal plate cells during the neural plate stage (1,322.8 +/- 28.8 ferritin particles/micron 2). As neural tube formation advanced, the number of receptors decreased as a result of an increase in the extent of the sparsely covered regions. The decrease in receptors for WGA occurred in a similar manner but more rapidly. By the stage of development at which the opposite sides of the neural ridges meet at the dorsal midline, the receptors for WGA were reduced to about half. After this period, the two lectin receptors did not show significant changes. This result suggests that sugar residues or the sugar-chain skeleton on basal plate cells are altered during neurulation.

Animals↗