The migration of neural crest cells to the wall of the digestive tract in avian embryo

Development ◽  
1973 ◽  
Vol 30 (1) ◽  
pp. 31-48
Author(s):  
Nicole M. Le Douarin ◽  
Marie-Aimée Teillet
Keyword(s):  
Neural Crest ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Avian Embryo ◽  
Somite Stage ◽  
Neuroblast Migration ◽  
Enteric Ganglia ◽  
Neural Axis ◽  
Hind Gut

Isotopic and isochronic grafts of quail neural primordium in chick embryos have been made. Due to the particular structure of their nuclei, quail cells can be distinguished from chick cells and so be used as natural markers to study the migration of neural crest cells. We have been able to demonstrate by this technique that the parasympathetic enteric ganglion cells arise from two different levels of the embryonic neural axis which correspond to the vagal and lumbo-sacral parasympathetic centres. The main source of the enteric neuroblasts is located at the level of the somites 1–7. It gives rise to ganglion cells which migrate in the whole gut including the large intestine and rectum. The other region from which enteric neuroblasts originate is situated behind the level of the 28th somite and gives rise only to some post-umbilical gut ganglion cells. In this region of the intestine the ganglia are made up of a mixture of cells arising from the vagal and the lumbo-sacral levels of the neural axis. The part of the neural primordium between the 8th and the 28th somite does not participate in the formation of the enteric ganglia. The chronology of the enteric neuroblast migration has been studied. Most cells of vagal origin leave the neural crest before the 13-somite stage but the migration lasts sometimes until after the 16-somite stage. Those cells which have to reach the hind-gut level accomplish a long-term migration which can be evaluated at 6 days or more. The presumptive neuroblasts of lumbo-sacral origin are not found in the hind-gut before the 7th day of incubation. In our experiments we have never observed the migration of any quail cells into the endoderm of the chick host embryo. Therefore we consider that enterochromaffin cells of the digestive epithelium are not derived from the levels of the neural crest concerned in these experiments (i.e. rhombencephalic and medullary Anlagen).

scholarly journals Further evidence that enterochromaffin cells are not derived from the neural crest

Development ◽  
1974 ◽  
Vol 31 (3) ◽  
pp. 589-598
Author(s):  
Ann Andrew
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Enterochromaffin Cells ◽  
Lateral Part ◽  
Time Of Arrival ◽  
Chick Embryos ◽  
Process Stage ◽  
Somite Stage ◽  
Enteric Ganglia ◽  
Probable Time

Recently, a previous finding that the enterochromaffin cells of chick embryos are not derived from the neural crest has been contested, and so further evidence has been sought. Presumptive gut, i.e. endoderm and adherent mesoderm, of embryos between the short head-process stage and the 25-somite stage was grown on the chorio-allantoic membranes of host embryos. Whether the presumptive gut was excised before or after the probable time of arrival of neural crest cells in the gut, enterochromaffin cells occurred in the intestine in the grafts. The presence or absence of enteric ganglia indicated the presence or absence, respectively, of neural crest cells. Enterochromaffin cells were plentiful even if the donor had been at a stage preceding that at which cells of the neural crest start to migrate, or preceding that at which the crests themselves first appear. In a second experiment, presumptive gut of embryos at 10- to 21-somite stages was excised so as to exclude the portion underlying the somites. Enteric ganglia were lacking in the intestine of these grafts, but enterochromaffin cells were invariably present. These experiments show that the precursors of enterochromaffin cells are present in the more lateral part of the presumptive gut before the neural crest precursors of enteric ganglia reach the region; and that they are present in the presumptive gut long before any crest cells could have arrived there. This evidence supports the view that enterochromaffin cells are not derived from the neural crest in chick embryos.

An experimental study on neural crest migration in Barbus conchonius (Cyprinidae, Teleostei), with special reference to the origin of the enteroendocrine cells

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 309-323
Author(s):  
C. H. J. Lamers ◽  
J. W. H. M. Rombout ◽  
L. P. M. Timmermans
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Enteroendocrine Cells ◽  
Pigment Cells ◽  
Transplantation Technique ◽  
Spinal Ganglion Cells ◽  
Neural Crest Origin ◽  
Neural Crest Migration

A neural crest transplantation technique is described for fish. As in other classes ofvertebrates, two pathways of neural crest migration can be distinguished: a lateroventral pathway between somites and ectoderm, and a medioventral pathway between somites and neural tube/notochord. In this paper evidence is presented for a neural crest origin of spinal ganglion cells and pigment cells, and indication for such an origin is obtained for sympathetic and enteric ganglion cells and for cells that are probably homologues to adrenomedullary and paraganglion cells in the future kidney area. The destiny of neural crest cells near the developing lateral-line sense organs is discussed. When grafted into the yolk, neural crest cells or neural tube cells appear to differentiate into ‘periblast cells’; this suggests a highly activating influence of the yolk. Many neural crest cells are found around the urinary ducts and, when grafted below the notochord, even within the urinary duct epithelium. These neural crest cells do not invade the gut epithelium, even when grafted adjacent to the developing gut. Consequently enteroendocrine cells in fish are not likely to have a trunkor rhombencephalic neural crest origin. Another possible origin of these cells will be proposed.

scholarly journals In Vivo Transplantation of Enteric Neural Crest Cells into Mouse Gut; Engraftment, Functional Integration and Long-Term Safety

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0147989 ◽  
Author(s):  
Julie E. Cooper ◽  
Conor J. McCann ◽  
Dipa Natarajan ◽  
Shanas Choudhury ◽  
Werend Boesmans ◽  
...  
Keyword(s):  
Neural Crest ◽  
Functional Integration ◽  
Neural Crest Cells

Pax3 is required for cardiac neural crest migration in the mouse: evidence from the splotch (Sp2H) mutant

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 505-514 ◽  
Author(s):  
S.J. Conway ◽  
D.J. Henderson ◽  
A.J. Copp
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Outflow Tract ◽  
Avian Embryo ◽  
Cardiac Neural Crest ◽  
Branchial Arches ◽  
Aortic Arches ◽  
Cardiac Outflow

Neural crest cells originating in the occipital region of the avian embryo are known to play a vital role in formation of the septum of the cardiac outflow tract and to contribute cells to the aortic arches, thymus, thyroid and parathyroids. This ‘cardiac’ neural crest sub-population is assumed to exist in mammals, but without direct evidence. In this paper we demonstrate, using RT-PCR and in situ hybridisation, that Pax3 expression can serve as a marker of cardiac neural crest cells in the mouse embryo. Cells of this lineage were traced from the occipital neural tube, via branchial arches 3, 4 and 6, into the aortic sac and aorto-pulmonary outflow tract. Confirmation that these Pax3-positive cells are indeed cardiac neural crest is provided by experiments in which hearts were deprived of a source of colonising neural crest, by organ culture in vitro, with consequent lack of up-regulation of Pax3. Occipital neural crest cell outgrowths in vitro were also shown to express Pax3. Mutation of Pax3, as occurs in the splotch (Sp2H) mouse, results in development of conotruncal heart defects including persistent truncus arteriosus. Homozygotes also exhibit defects of the aortic arches, thymus, thyroid and parathyroids. Pax3-positive neural crest cells were found to emigrate from the occipital neural tube of Sp2H/Sp2H embryos in a relatively normal fashion, but there was a marked deficiency or absence of neural crest cells traversing branchial arches 3, 4 and 6, and entering the cardiac outflow tract. This decreased expression of Pax3 in Sp2H/Sp2H embryos was not due to down-regulation of Pax3 in neural crest cells, as use of independent neural crest markers, Hoxa-3, CrabpI, Prx1, Prx2 and c-met also revealed a deficiency of migrating cardiac neural crest cells in homozygous embryos. This work demonstrates the essential role of the cardiac neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that Pax3 function is required for the cardiac neural crest to complete its migration to the developing heart.

The developmental fate of the cephalic mesoderm in quail-chick chimeras

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 1-15 ◽  
Author(s):  
G.F. Couly ◽  
P.M. Coltey ◽  
N.M. Le Douarin
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Facial Skeleton ◽  
Developmental Fate ◽  
Prechordal Mesoderm ◽  
The Face ◽  
Neural Crest Origin ◽  
Neurula Stage

The developmental fate of the cephalic paraxial and prechordal mesoderm at the late neurula stage (3-somite) in the avian embryo has been investigated by using the isotopic, isochronic substitution technique between quail and chick embryos. The territories involved in the operation were especially tiny and the size of the transplants was of about 150 by 50 to 60 microns. At that stage, the neural crest cells have not yet started migrating and the fate of mesodermal cells exclusively was under scrutiny. The prechordal mesoderm was found to give rise to the following ocular muscles: musculus rectus ventralis and medialis and musculus oblicus ventralis. The paraxial mesoderm was separated in two longitudinal bands: one median, lying upon the cephalic vesicles (median paraxial mesoderm—MPM); one lateral, lying upon the foregut (lateral paraxial mesoderm—LPM). The former yields the three other ocular muscles, contributes to mesencephalic meninges and has essentially skeletogenic potencies. It contributes to the corpus sphenoid bone, the orbitosphenoid bone and the otic capsules; the rest of the facial skeleton is of neural crest origin. At 3-somite stage, MPM is represented by a few cells only. The LPM is more abundant at that stage and has essentially myogenic potencies with also some contribution to connective tissue. However, most of the connective cells associated with the facial and hypobranchial muscles are of neural crest origin. The more important result of this work was to show that the cephalic mesoderm does not form dermis. This function is taken over by neural crest cells, which form both the skeleton and dermis of the face. If one draws a parallel between the so-called “somitomeres” of the head and the trunk somites, it appears that skeletogenic potencies are reduced in the former, which in contrast have kept their myogenic capacities, whilst the formation of skeleton and dermis has been essentially taken over by the neural crest in the course of evolution of the vertebrate head.

Spatial and temporal distribution of vinculin and talin in migrating avian neural crest cells and their derivatives

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 421-433
Author(s):  
J.L. Duband ◽  
J.P. Thiery
Keyword(s):  
Neural Crest ◽  
Expression Patterns ◽  
Temporal Distribution ◽  
Neural Crest Cells ◽  
Cell Types ◽  
Avian Embryo ◽  
Sensory Ganglia ◽  
Adhesive Properties ◽  
Final Destination ◽  
Derivatives Of

Neural crest cells express different adhesion modes at each phase of their development starting with their separation from the neural tube, followed by migration along definite pathways throughout the embryo, and finally to settlement and differentiation in elected embryonic regions. In order to determine possible changes in the cytoskeleton organization and function during these processes, we have studied the in situ distribution of two major cytoskeleton-associated elements involved in the membrane anchorage of actin microfilaments, i.e. vinculin and talin, during the ontogeny of the neural crest and its derivatives in the avian embryo. Prior to emigration, neural crest cells exhibited both vinculin and talin at levels similar to the neighbouring neural epithelial cells, and this expression apparently did not change as cells became endowed with migratory properties. However, vinculin became selectively enhanced in neural crest cells as they further migrated towards their final destination. This increase in vinculin amount was particularly striking in vagal and truncal neural crest cells entering cellular environments, such as the sclerotome and the gut mesenchyme. Talin was also expressed by neural crest cells but, in contrast to vinculin, staining was not conspicuous compared to neighbouring mesenchymal cells. High levels of vinculin persisted throughout embryogenesis in almost all neural derivatives of the neural crest, including the autonomous and sensory ganglia and Schwann cells along the peripheral nerves. In contrast, the non-neural derivatives of the neural crest rapidly lost their prominent vinculin staining after migration. The pattern of talin in the progeny of the neural crest was complex and varied with the cell types: for example, some cranial sensory ganglia expressed high amounts of the molecule whereas autonomic ganglia were nearly devoid of it. Our results suggest that (i) vinculin and talin may follow independent regulatory patterns within the same cell population, (ii) the level of expression of vinculin and talin in neural crest cells may be consistent with the rapid, constant modulations of their adhesive properties, and (iii) the expression patterns of the two molecules may also be correlated with the genesis of the peripheral nervous system.

scholarly journals Cranial neural crest cells form corridors prefiguring sensory neuroblast migration

Development ◽  
2013 ◽  
Vol 140 (17) ◽  
pp. 3595-3600 ◽  
Author(s):  
S. Freter ◽  
S. J. Fleenor ◽  
R. Freter ◽  
K. J. Liu ◽  
J. Begbie
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Neuroblast Migration ◽  
Cranial Neural Crest Cells

scholarly journals Tissue interactions affecting the migration and differentiation of neural crest cells in the chick embryo

Development ◽  
1991 ◽  
Vol 113 (1) ◽  
pp. 207-216 ◽  
Author(s):  
C.D. Stern ◽  
K.B. Artinger ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Dorsal Root ◽  
Ganglion Cells ◽  
Neural Crest Cells ◽  
Motor Axons ◽  
Root Region ◽  
Tissue Interactions ◽  
Catecholamine Fluorescence ◽  
Catecholaminergic Cells

A series of microsurgical operations was performed in chick embryos to study the factors that control the polarity, position and differentiation of the sympathetic and dorsal root ganglion cells developing from the neural crest. The neural tube, with or without the notochord, was rotated by 180 degrees dorsoventrally to cause the neural crest cells to emerge ventrally. In some embryos, the notochord was ablated, and in others a second notochord was implanted. Sympathetic differentiation was assessed by catecholamine fluorescence after aldehyde fixation. Neural crest cells emerging from an inverted neural tube migrate in a ventral-to-dorsal direction through the sclerotome, where they become segmented by being restricted to the rostral half of each sclerotome. Both motor axons and neural crest cells avoid the notochord and the extracellular matrix that surrounds it, but motor axons appear also to be attracted to the notochord until they reach its immediate vicinity. The dorsal root ganglia always form adjacent to the neural tube and their dorsoventral orientation follows the direction of migration of the neural crest cells. Differentiation of catecholaminergic cells only occurs near the aorta/mesonephros and in addition requires the proximity of either the ventral neural tube (floor plate/ventral root region) or the notochord. Prior migration of presumptive catecholaminergic cells through the sclerotome, however, is neither required nor sufficient for their adrenergic differentiation.

scholarly journals Neural tube-ectoderm interactions are required for trigeminal placode formation

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4287-4295 ◽  
Author(s):  
M.R. Stark ◽  
J. Sechrist ◽  
M. Bronner-Fraser ◽  
C. Marcelle
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Surface Ectoderm ◽  
Somite Stage ◽  
Tissue Interactions ◽  
Cranial Neural Crest Cells ◽  
Cranial Sensory Ganglia ◽  
Placode Formation

Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode.

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