Visceral Arches Research Articles

Specific responsiveness of chick trigeminal motor nucleus explants to target-conditioned media.

Explants of the neural tube from stage 11 chick embryos containing the metencephalic trigeminal (V) motor nucleus were cultured in standard control medium, in medium conditioned by appropriate target musculature (the mandibular process of the first visceral arch that gives rise to jaw musculature innervated by motor V) or in medium conditioned by inappropriate target musculature (rostral limb bud tissue). The appropriate and inappropriate muscle tissues were of the same developmental stage (stage 22) and were in similar states of differentiation. At this point in vivo, both are just beginning to be innervated. The neuritic outgrowth from the explants was quantified after 6 days in vitro. While explants from all three groups appeared healthy and exhibited some neuritic outgrowth, the density and complexity of this growth was significantly greater in the group cultured with the appropriate (jaw) muscle-conditioned medium. Growth in this group significantly surpassed that of both the control and the inappropriate muscle-conditioned medium group did not differ from the control group. These results demonstrate a specific responsiveness of the trigeminal motor nucleus population to its appropriate target tissue. Since relatively small amounts of the muscle-conditioned medium were used with each explant, it is suggested that there is a high degree of sensitivity of this population to factors present in their target at the time innervation would normally be occurring. It is hypothesized that such selective responsiveness may play a role in guiding or sustaining growth during normal neurogenesis.

Fetal alcohol syndrome and DiGeorge anomaly: critical ethanol exposure periods for craniofacial malformations as illustrated in an animal model.

Acute maternal ethanl (alcohol) administration induces different craniofacial anomalies in the offspring of experimental animals, depending on the gestational day of teratogen exposure. Previous studies in our laboratories have illustrated the sequence of developmental changes leading to the "typical" fetal alcohol syndrome (FAS) craniofacial phenotype which results from teratogen exposure during gastrulation. These facial features are accompanied by deficiencies in median forebrain derivatives. Ethanol teratogenesis at this time apparently results in a loss of midline territory of the embryonic disc with little effects on neural crest-dependent laterally derived structures including the visceral arches. Acute ethanol exposure in mice 1 1/2 days later, at a time when neural crest cells are populating the frontonasal prominence and the visceral arches, results in a craniofacial phenotype that is similar to that noted in the DiGeorge anomaly or sequence. Sequential scanning electron microscopic analysis in our laboratory of embryos exposed on day 8 1/2 have illustrated deficiencies in the developing facial prominences and the visceral arches. The developing forebrain and midbrain appear hypoplastic. We have also observed heart, great vessel, and thymus abnormalities in these fetuses. Histologic analyses indicate that a common pathogenetic basis for the above-mentioned (day 8 1/2-induced) fetal alcohol effects appears to be an interference with the integrity of the cranial (including occipital) neural crest. Other discrete cell populations may also be involved since we have observed abnormalities in other regions, including placodal and closing membrane tissues. This animal model provides evidence linking maternal ethanol abuse during the 3rd or 4th weeks of human gestation to the development in the conceptus of FAS or DiGeorge anomally craniofacial characteristics, respectively. As the DiGeorge anomaly has been noted in the offspring of alcoholic women, this animal model indicates that ethanol and/or its metabolites is, in these cases, the causative agent.

The development and distribution of the cranial neural crest in the rat embryo.

The head region of rat embryos was investigated by scanning electron microscopy after removal of the surface ectoderm with adhesive tape. Observations were made in embryos from 6-somite to 11-somite stages of development, in order to determine: (1) the sequence of emigration of neural crest cells from the different regions of the future brain; (2) the appearance of crest cells before, during, and after their conversion from an epithelial to a mesenchymal form; (3) the migration pathways. Emigration occurs first from the midbrain, and next from the rostral hindbrain; crest cells from these two regions migrate into the first visceral arch. Subsequently cells emigrate from the caudal hindbrain, but not in a rostrocaudal sequence. At the time of crest cell emigration, the neural fold morphology varies from a slightly convex, widely open plate (midbrain) to a closed tube (caudal hindbrain). Thus the timing of emigration is related neither to age (as reflected in rostrocaudal levels) nor to morphology of the neural epithelium.

Interruption of the aortic arch and coarctation of the aorta: Pathogenetic relations

The pathologic anatomic features and associated cardiac anomalies of 63 cases of interruption of the aortic arch (IAA) type A (54 reported and 9 observed) and 145 cases of type B (124 reported and 21 observed) were analyzed and compared with those seen in 57 autopsy cases of infant coarctation of the aorta (CA). There was no significant sex predominance within the 3 groups and the prognosis without surgery was uniformly poor. Ventricular septal defect was much more common in IAA type B than in type A or CA. Anomalous origin of the subclavian artery and DiGeorge syndrome were commonly associated with IAA type B but were rare in type A and CA. Transposition of the great arteries and double-inlet left ventricle are less common in IAA type B than in types A and CA. On the basis of these findings and the observation by Le Lièvre and Le Douarin that neural crest cells contribute significantly to the formation of the visceral arch system and associated organs, we postulate that IAA type B may be a manifestation of a developmental error involving the neural crest, as is the DiGeorge syndrome. We believe IAA type A and CA to be closely related anomalies that may be prenatally acquired and pathogenetically distinct from IAA type B.

Bilateral choanal atresia in two members of one family

Two children are presented with bilateral choanal atresia: a girl with the typical features of the Treacher Collins syndrome, and a boy, a third cousin of the girl, without mandibulo-facial dysostosis. Simultaneous occurrence of choanal atresia and the Treacher Collins syndrome may be based on a defective ossification of the mesenchyme of the first visceral arch. Choanal atresia may be due to nonabsorption of the bucconasal membrane and/or extension of the sphenoid or palate bone.

A scanning electron microscopic study of the development of the shoulder, visceral arches, and the region ventral to the cervical somites of the chick embryo

Scanning electron microscopy (SEM) was used to investigate the development of the shoulder in the chick embryo. Initially the wing grows on an axis perpendicular to the dorso-ventral and cranial-caudal axes of the embryo, but soon begins to grow in a ventral and partially caudal direction. The change in axis of outgrowth occurs while the shoulder forms at the cranial proximal portion of the wing. Analysis of SEM observations, together with an analysis of serially sectioned embryos and photographs of live embryos in ovo has demonstrated that the shoulder continues to grow out on an axis perpendicular to the dorso-ventral axis of the embryo, while the caudal and distal portions of the wing grow ventrally. The change in axis of outgrowth seems to be due to 1) the formation of the viscera under the wing, 2) the closing of the membrana reuniens to form a continuous sheet covering the viscera under the wing. 3) caudal movement of the duct of Cuvier and the cranial margin of the pleural coelom, and 4)ventral movement of the lateral body fold caudal to the wing. Although the visceral arches undergo major morphogenetic changes during this period, the visceral arches do not appear to have an influence on shoulder development.

Early development and migration of the trigeminal motor nucleus in the chick embryo.

The development of the trigeminal motor nucleus in the chick embryo was studied using autoradiographic, cell staining, fiber staining, and axonal transport techniques. It was found that this nucleus arises very early in neurogenesis, with the first cells produced at 48 hours of incubation (stage 12), peak cell production at 50--56 hours (stage 15), and neuroblast proliferation completed by 72 hours (stage 18). As has been described in mammalian embryos, the primordial trigeminal cells move from the ventricular layer to accumulate as part of the common medial column, and later migrate in a ventrolateral direction to form the definitive lateral motor nucleus. The first identifiable component of the trigeminal system is the semilunar ganglion, which flanks the neural tube at stage 12, and sends afferents into the metencephalon by stage 13. By stage 12-13, the medial column cells are first apparent, and at stage 14, a few of these medial column cells have moved to begin formation of a lateral nucleus. At this time, a thin motor root can be seen exiting the brainstem. During subsequent stages, migratory traffic from medial to lateral regions increases, with cells frequently moving in association with fiber processes in the marginal zone. These fibers are presumed to emanate from secondary sensory, reticular, and medial column neuroblasts. By day 5, the medial column is greatly depleted and by day 6--7, the definitive lateral motor nucleus is formed. Beginning at 5 days, the dorsal motor nucleus can be detected, with cells from the lateral nucleus appearing to stream in a dorsomedial direction for its formation. Injections of horseradish peroxidase (HRP) into the mandibular process of the first visceral arch resulted in retrograde labeling of lateral nucleus cells as early as 3.5 days of incubation. In addition, migrating cells, intermediate between medial column and lateral nucleus, were similarly labeled. These observations indicate that processes of the lateral nucleus cells and those of migrating cells are well into their peripheral field at this age, but we cannot conclude that neuromuscular affiliations have been established, due to the possibility of HRP diffusion and growth cone uptake.

The control of avian cephalic neural crest cytodifferentiation: I. Skeletal and connective tissues

The neural crest is the embryonic source of many skeletal and connective tissues associated with the visceral arches of vertebrate embryos. By transplanting quail premigratory neural crest cells, which contain a distinctive nuclear marker [Le Douarin, N. M. (1971). Ann. Embryol. Morphol. 4, 125–135], orthotopically into various preotic regions of the chick, it has been shown that all cartilages and bones and most connective tissues of the facial and oral regions are of crest cell origin. These derivatives include the frontal, prefrontal, nasal, maxilla, premaxilla, parasphenoid, palatine, pterygoid, and squamosal bones, in addition to lower jaw skeletal elements. Most connective tissues found in the facial and periprosencephalic regions are of crest origin, including the corneal endothelium, stromal cells, and leptomeningeal tissues. To examine whether crest cells were restricted to specific developmental pathways, quail crest cells from one part of the head were grafted in the place of a different population of chick crest cells. In all cases these host embryos were identical to controls, indicating that cytodifferentiation, growth, and histogenesis of crest-derived tissues are directed by environmental influences encountered by migrating crest cells after they leave their origin.

Peripheral innervation by migrating neuroblasts in the chick embryo

Horseradish peroxidase (HRP) was injected into the mandibular process of the first visceral arch in chick embryos of 3–6 days of incubation. On days 3 1 2 , 4 and 4 1 2 of incubation, this procedure resulted in granular reaction product in neuroblasts of the lateral trigeminal nucleus and in soma and processes of neuroblasts in the process of migrating from the medial column to form the lateral nucleus. On days 5 and 6 of incubation, similar labeling was found in cells migrating from the lateral nucleus dorsal to form the dorsal trigeminal nucleus. This is the first clear demonstration of the extent of differentiation which may take place during neurogenesis prior to the completion of migration.

A histological study of the development of the avian middle ear and tympanum.

The development of the middle ear and tympanum of Gallus gallus has been studied in embryos Hamilton-Hamburger stages 20-46. Particular attention was paid to the pattern of expansion of the pharyngeal pouch forming the tympanic cavity, and the histogenesis of the tissues of the region of the vestibular window. It is concluded that pouch expansion is brought about by simple epithelial growth into regions devoid of mesenchyme. The mesenchyme does not show significant cell death, but differentiates as connective tissue, macrophages, and sinus vascular spaces. The epithelium of the mature cavity is of endodermal origin, and there is no indication of celomic contributions. We provide a detailed morphological analysis of the development of the footplate from cells of both the second visceral arch and the otic capsule. These detailed observations on the patterns of chondrification of columella and capsular tissues permit the presentation of a model for cellular interactions leading to the differentiation of the annular ligament.

Inhibition of cranial neural crest cell development by vitamin A in the cultured chick embryo

Chick embryos at stage 8, prior to neural crest cell migration, were explanted on whole egg medium with or without vitamin A and cultured for 3 days. Sections through the head regions showed that the cranial neural crest cells had migrated into the first visceral arch in the controls but were absent from this structure in the treated embryos. These observations suggest that vitamin A inhibits neural crest cell development or migration, an effect which may in part account for the facial malformations produced by excess vitamin A.

Mobius Syndrome and Limb Abnormalities

Most ophthalmologists are aware of the cranial nerve dysfunctions that have been associated with the facial diplegias of Mobius syndrome. However, many are not aware of the combined limb deficiencies and cranial nerve dysfunctions. Limb malformations have been associated with a spectrum of oral facial anomalies consisting of micrognathia, hypoglossia, microstomia, hypodontia, oral bands, and dysarthria. It has been suggested that the differences which exists between these entities may in fact represent a common etiology. The variability may be related to an intrauterine insult at slightly different times. The oral-facial anomalies associated with absence of limbs or of limb anomalies suggests a correlation between the limbs and the first visceral arch possibly within the second month of gestation.

A Theory Concerning the Early Evolution of the Visceral Arches

AbstractThe visceral arches are usually assumed to develop in a similar way, from front to rear, with corresponding parts. The mandibular and hyoid arches do not follow such a pattern, rather some of the blastematic tissue of these arches became involved in the formation of the neurocranium as the trabecula and lateral commissure respectively. Thus this tissue was never developed as arch elements. Further, skeletal blastemas in the head are derived from delamination as well neural crest. The implications of these observations are explored.

Anomalies in derivatives from the visceral arches combined with congenital heart defects.

In a series of 20 patients with tetralogy of Fallot and some other complicated congenital heart defects, anomalies in derivatives from the visceral arches were recorded. A high frequency of dental malocclusion and external ear anomalies was found. The study also indicated an increased activity of dental caries. All the patients had postural defects, and some aspects of these findings are discussed. The significance of the combination of these defects in relation to teratology and embryo-pathology in general should be borne in mind.

The syndrome of congenital ptosis and developmental abnormalities of the first visceral arch.

SUMMARYThe author describes three patients with congenital ptosis and malformation of structures derived from the mandibular arch. These abnormalities are probably determined by a single genetic defect with autosomal dominant transmission and variable expressivity.RÉSUMÉCet article contient une description de trois malades avec ptosis congenital et malformations des structures dérivées de l'arc mandibulaire. Ces anomalies sont probablement déterminées par un seul défaut génétique à transmission dominante autosomale et à expression variable.RESUMENEl autor describe a tres enfermos afectos de ptosis congénita y de malformación de estructuras derivadas del arco mandibular. Estas malformaciones son determinadas probablemente por un solo defecto genético con transmisión autosomal dominante y expresión variable.

Stability of chondrocyte differentiation and contribution of muscle to cartilage during limb regeneration in the axolotl (Siredon mexicanum).

AbstractIn order to determine whether chondrocytes are stable as to type during limb regeneration and whether any cells from limb muscle become chondrocytes in the regenerate, labeled cartilage and muscle were transplanted into limbs which were then allowed to regenerate. Transplanted cells were identified after redifferentiation in the regenerate by three kinds of label: H3‐thymidine detected by radioautography; triploidy as judged by the presence of three nucleoli per nucleus; or a combination of the two.The results of this investigation indicate that limb chondrocytes are intrinsically stable with respect to cell type, for grafts of both triploid and H3‐thymidine labeled chondrocytes gave rise to morphologically dedifferentiated blastema cells which almost exclusively differentiated into chondrocytes. The small percentage of labeled noncartilage cells observed could have been the result of metaplasia, although it is more likely that all or most of them arose as spontaneous polyploids or as contaminants of the original grafts. Isotope dilution in H3‐thymidine labeled chondrocytes indicated that they had usually divided at least five times. Hence, the basis for the intrinsic stability of chondrocytes must be heritable.Chondrocytes from the coracoid, scapula, and visceral arch cartilages also contributed cells to cartilage of limb regenerates, and the available evidence indicates that cells released from these cartilages are similarly stable as to type. These cartilages did not dedifferentiate and participate in limb regeneration to the same extent as did limb cartilage.Results from transplanted limb muscle, labeled by all three methods used in this study, indicate that certain cells of muscle can become chondrocytes during limb regeneration. The exact cellular origin of these chondrocytes, however, is uncertain, for muscle is a mixture of cell types.

A radioautographic study of the migration and fate of cranial neural crest cells in the chick embryo.

AbstractThe migration and fate of cranial neural fold cells of the chick embryo (White Leghorn strain) were followed radioautographically after replacing crestcontaining fold segments with comparable segments from donor embryos labeled with tritiated thymidine. The behavior of the neural crest cells was found to be remarkably similar to that of their amphibian counterparts. The movements of labeled crest cells into the upper facial region of the chick embryo, in conjunction with their proliferative activity, apparently gave rise to the embryonic facial (medial and lateral nasal, and maxillary) processes. As the cells moved into the visceral arches, they surrounded the core‐ like mescdermal muscle plates.In the upper face and visceral arch regions, labeled crest cells participated in the formation of cartilage. Judging from the distribution of these cells in the remaining mesenchyme, it appears that the still undifferentiated skeletal and connective tisues of these regions are also of neural crest origin. Labeled crest cells were also found in the root ganglia of the VIIth and of the IXth and Xth nerves and the trigeminal and ciliary ganglia. While labeled neural crest contributed extensively to the formation of sheath cells, it made rather limited contributions to the meninges of the brain.

The relationship of viral antigen to virus-induced defects in chick embryos. Newcastle disease virus

Results indicate that the developmental defects observed in chick embryos following inoculation of Newcastle disease virus at 36, 48, and 60 hours' incubation are due to sloughing and necrosis of cells in specifically differentiating organs following replication of viral antigen in cells of such tissues. Although replication of viral antigen is not limited to these structures, minimal cell damage is observed in other structures within the time limits of the study. Using immunofluorescent staining techniques, the viral antigen is consistently observed first, at 6–8 hours postinoculation, in cells of the extraembryonic structures, i.e., ectoderm of somatopleure and amnion and endoderm of splanchnopleure. In tissues of the embryo, specific fluorescence begins to appear at 10–12 hours postinoculation; it is first concentrated in structures differentiating from the body ectoderm. The pattern of fluorescence conforms in general to structures previously observed to be susceptible to teratogenic effects or microscopic pathological changes. Structures consistently affected include lens, auditory epithelium, visceral arch ectoderm, olfactory epithelium, and caudal neural tube. The optic cups and the brain, which is closed off and separated from the body ectoderm at the time of inoculation, show no evidence of infection. As infection progresses the specific fluorescence is observed in more of the general body ectoderm and invasion is also observed in the underlying mesoderm, where it is located chiefly in visceral arches, somites, epimyocardium of the heart, and endothelium of capillaries that lie in affected areas of the mesoderm.

Early development of the head and pharynx of Neoceratodus with a consideration of its phylogeny

The development of the head and pharynx of larvae of Neoceratodus (ranging in length from 11.5 to 34. 5 mm) was investigated form microscopic transverse serial sections. The structures studied included the chondrocranium and visceral arches, ossifications, cranial and anterior spinal nerves, musculature and vascular system. These components of Neoceratodus are compared with similar ones, likewise investigated, in Rana temporaria and Rana esculenta (33 and 26 mm long, respectively), and in various genera of Urodela, either previously investigated by the author or by reference to the earlier literature.Some new homologues of the various morphological components of the head and pharynx of these groups are suggested.On the basis of the larval structure an assessment is made of the classical view of a close phylogenetic relationship between Neoceratodus and the two amphibian groups. it is concluded that they share a common derivation from pro‐dipnoan‐amphibian stock—of crossopterygian ancestry—in the early Devonian: a conclusion which supports an earlier somewhat similar view of Goodrich.It is further considered that there is evidence of a quasi parallel evolution between Neoceratodus and Urodela, though some assumed similarities in larval structure are spurious; nevertheless, in some ways, they are more similar than are Neoceratodus and members of the Anura.A common origin of Neoceratodus (Dipnoi) and the amphibian groups supports the vie of a monophyletic derivation of the Tetrapoda.

ANATOMY AND CLINICAL ASPECTS OF THE FACIAL NERVE.

THE CONVOLUTED course of the seventh nerve through the ear can be described with a grain of salt as constant. Changes in its anatomy have so far been described as relatively rare. Apart from dehiscences of the fallopian canal which should not be regarded as anomalies even though they sometimes are very extensive, there are frequent anomalies of the anatomical course which can be of clinical significance (see Fowler, Kettel, Angell-James, and Behrens). Moreover, Fowler, Jr., Hawley, Hahlbrock, Kettel, Basek, and I saw bipartition of the nerve, and Jongkees even saw a tripartition. All these anomalies were found in patients with completely normal aural findings. On the other hand, changes in course exceeding the anomalies just mentioned are generally associated with malformations of the ear, for the facial nerve as a derivative of the second branchial arch during ontogenesis is closely adjacent to the derivatives of the first visceral arch