Mouse-chick chimera: a developmental model of murine neurogenic cells

Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3025-3036 ◽  
Author(s):  
J. Fontaine-Perus ◽  
P. Halgand ◽  
Y. Cheraud ◽  
T. Rouaud ◽  
M.E. Velasco ◽  
...  
Keyword(s):  
Nervous System ◽  
Neural Tube ◽  
Mammalian Cells ◽  
Mouse Embryos ◽  
Developmental Model ◽  
Sensory Ganglia ◽  
Chick Embryos ◽  
In Ovo ◽  
Neuroepithelial Cells ◽  
Cellular Compartments

Chimeras were prepared by transplanting fragments of neural primordium from 8- to 8.5- and 9-day postcoital mouse embryos into 1.5- and 2-day-old chick embryos at different axial levels. Mouse neuroepithelial cells differentiated in ovo and organized to form the different cellular compartments normally constituting the central nervous system.The graft also entered into the development of the peripheral nervous system through migration of neural crest cells associated with mouse neuroepithelium. Depending on the graft level, mouse crest cells participated in the formation of various derivatives such as head components, sensory ganglia, orthosympathetic ganglionic chain, nerves and neuroendocrine glands. Tenascin knockout mice, which express lacZ instead of tenascin and show no tenascin production (Saga, Y., Yagi, J., Ikawa, Y., Sakakura, T. and Aizawa, S. (1992) Genes and Development 6, 1821–1838), were specifically used to label Schwann cells lining nerves derived from the implant. Although our experiments do not consider how mouse neural tube can participate in the mechanism required to maintain myogenesis in the host somites, they show that the grafted neural tube behaves in the same manner as the chick host neural tube. Together with our previous results on somite development (Fontaine-Perus, J., Jarno, V., Fournier Le Ray, C., Li, Z. and Paulin, D. (1995) Development 121, 1705–1718), this study shows that chick embryo constitutes a privileged environment, facilitating access to the developmental potentials of normal or defective mammalian cells. It allows the study of the histogenesis and precise timing of a known structure, as well as the implication of a given gene at all equivalent mammalian embryonic stages.

scholarly journals Vital dye labelling demonstrates a sacral neural crest contribution to the enteric nervous system of chick and mouse embryos

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 857-866 ◽  
Author(s):  
G.N. Serbedzija ◽  
S. Burgan ◽  
S.E. Fraser ◽  
M. Bronner-Fraser
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Mouse Embryos ◽  
Chick Embryos ◽  
Vital Dye ◽  
Dorsal Portion ◽  
Sacral Neural Crest

We have used the vital dye, DiI, to analyze the contribution of sacral neural crest cells to the enteric nervous system in chick and mouse embryos. In order to label premigratory sacral neural crest cells selectively, DiI was injected into the lumen of the neural tube at the level of the hindlimb. In chick embryos, DiI injections made prior to stage 19 resulted in labelled cells in the gut, which had emerged from the neural tube adjacent to somites 29–37. In mouse embryos, neural crest cells emigrated from the sacral neural tube between E9 and E9.5. In both chick and mouse embryos, DiI-labelled cells were observed in the rostral half of the somitic sclerotome, around the dorsal aorta, in the mesentery surrounding the gut, as well as within the epithelium of the gut. Mouse embryos, however, contained consistently fewer labelled cells than chick embryos. DiI-labelled cells first were observed in the rostral and dorsal portion of the gut. Paralleling the maturation of the embryo, there was a rostral-to-caudal sequence in which neural crest cells populated the gut at the sacral level. In addition, neural crest cells appeared within the gut in a dorsal-to-ventral sequence, suggesting that the cells entered the gut dorsally and moved progressively ventrally. The present results resolve a long-standing discrepancy in the literature by demonstrating that sacral neural crest cells in both the chick and mouse contribute to the enteric nervous system in the postumbilical gut.

Teratogenic activity of methadone hydrochloride in mouse and chick embryos

Development ◽  
1973 ◽  
Vol 30 (2) ◽  
pp. 449-458
Author(s):  
A. Jurand
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Neural Plate ◽  
Mouse Embryos ◽  
Chick Embryos ◽  
In Ovo ◽  
Cervical Area ◽  
Extensive Necrosis

Teratogenic activity of methadone HCl (Physeptone, Burroughs Wellcome and Co.) was tested on inbred JBT/Jd and outbred Q strain mouse embryos and on chick embryos. 22–24 mg/kg injected subcutaneously on the 9th day of pregnancy caused by the 13th day exencephaly in 56 out of 479 JBT/Jd embryos but after 32 mg/kg only in 1 out of 220 of the Q strain. Some affected JBT/Jd embryos showed also rachischisis in the cervical area. The second abnormality shown by the embryos of both strains is Z-shaped kinkage of the spinal cord. In explanted chick embryos cultured in vitro as well as in embryos treated in ovo methadone causes non-closure of the neural tube with extensive necrosis of the neural plate cells in the cephalic region. The results of this study indicate that methadone, which is a neutropic drug, has an embryotoxic activity directed against the developing central nervous system.

Optogenetic regulation of leg movement in midstage chick embryos through peripheral nerve stimulation

2011 ◽  
Vol 106 (5) ◽  
pp. 2776-2782 ◽  
Author(s):  
Andrew A. Sharp ◽  
Sylvia Fromherz
Keyword(s):  
Nervous System ◽  
Neuronal Activity ◽  
Expression System ◽  
Continuous Illumination ◽  
Chick Embryos ◽  
Motor Axons ◽  
In Ovo ◽  
Full Extension ◽  
Sensorimotor Development ◽  
Spontaneous Movements

Numerous disorders that affect proper development, including the structure and function of the nervous system, are associated with altered embryonic movement. Ongoing challenges are to understand in detail how embryonic movement is generated and to understand better the connection between proper movement and normal nervous system function. Controlled manipulation of embryonic limb movement and neuronal activity to assess short- and long-term outcomes can be difficult. Optogenetics is a powerful new approach to modulate neuronal activity in vivo. In this study, we have used an optogenetics approach to activate peripheral motor axons and thus alter leg motility in the embryonic chick. We used electroporation of a transposon-based expression system to produce ChIEF, a channelrhodopsin-2 variant, in the lumbosacral spinal cord of chick embryos. The transposon-based system allows for stable incorporation of transgenes into the genomic DNA of recipient cells. ChIEF protein is detectable within 24 h of electroporation, largely membrane-localized, and found throughout embryonic development in both central and peripheral processes. The optical clarity of thin embryonic tissue allows detailed innervation patterns of ChIEF-containing motor axons to be visualized in the living embryo in ovo, and pulses of blue light delivered to the thigh can elicit stereotyped flexures of the leg when the embryo is at rest. Continuous illumination can disrupt full extension of the leg during spontaneous movements. Therefore, our results establish an optogenetics approach to alter normal peripheral axon function and to probe the role of movement and neuronal activity in sensorimotor development throughout embryogenesis.

scholarly journals Analysis of the effects of Streptomyces hyaluronidase on formation of the neural tube

Development ◽  
1983 ◽  
Vol 73 (1) ◽  
pp. 1-15
Author(s):  
Gary C. Schoenwolf ◽  
Marilyn Fisher
Keyword(s):  
Spinal Cord ◽  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Developmental Process ◽  
Chick Embryos ◽  
In Ovo ◽  
Dorsal Midline ◽  
Specific Protease

Chick embryos at stages 8 to 9 were treated in ovo with Streptomyces hyaluronidase (SH) to determine whether neurulation occurs normally in embryos depleted of hyaluronic acid, a major component of the extracellular matrix. Open neural tube defects occurred in 60–94 % (depending on the particular enzyme batch) of the embryos treated with SH and examined after an additional 24 h of incubation. Defects were confined mainly to the spinal cord. The neural folds underwent elevation in defective regions but failed to converge and fuse across the dorsal midline. The extracellular matrix of embryos treated with SH was depleted consistently, as determined with sections stained with Alcian blue. Control experiments were done to ensure that neural tube defects were not caused by non-specific protease contamination of SH, or by digestion products of hyaluronic acid. We propose several plausible and testable mechanisms through which the extracellular matrix might influence the complex developmental process of neurulation.

Experiments on the ‘Overgrowth’ Phenomenon in the Brain of Chick Embryos

Development ◽  
1959 ◽  
Vol 7 (2) ◽  
pp. 122-127
Author(s):  
Harry Bergquist
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neural Tube ◽  
Human Embryos ◽  
Chick Embryos ◽  
Cranial Cavity ◽  
The Central Nervous System ◽  
The Brain ◽  
Rostral Part ◽  
Exact Term

Patten (1952) described ‘a curious distortion of the central nervous system’ in human embryos measuring 5, 7, 12·5, 20, and 30 mm. in length, as well as in some pig embryos. The malformation was called ‘overgrowth of the neural tube’. Instead of the indecisive word ‘overgrowth’ the present writer suggests the more exact term ‘hypermorphosis’ should be used for this malformation. Patten described it in the following way: ‘the neural tube epithelium had started to grow wildly so that it became folded, and refolded on itself, as if it was crowded into a cranial space fairly normal in size and shape’. The phenomenon was most distinctly developed in the rostral part of the neural tube. In some cases the cranial cavity was expanded by the process, giving rise to a high-crowned skull. In other cases an encephalocoel was formed. In later papers (1953, 1957) Patten discussed this phenomenon further.

Relationship between Wnt-1 and En-2 expression domains during early development of normal and ectopic met-mesencephalon

Development ◽  
1992 ◽  
Vol 115 (4) ◽  
pp. 999-1009 ◽  
Author(s):  
L. Bally-Cuif ◽  
R.M. Alvarado-Mallart ◽  
D.K. Darnell ◽  
M. Wassef
Keyword(s):  
In Situ Hybridization ◽  
Neural Tube ◽  
Expression Patterns ◽  
Mouse Embryos ◽  
Chick Embryos ◽  
Expression Domain ◽  
General Role ◽  
Maximal Expression

Grafting a met-mesencephalic portion of neural tube from a 9.5-day mouse embryo into the prosencephalon of a 2-day chick embryo results in the induction of chick En-2 (ChickEn) expression in cells in contact with the graft (Martinez et al., 1991). In this paper we investigate the possibility of Wnt-1 being one of the factors involved in En-2 induction. Since Wnt-1 and En-2 expression patterns have been described as diverging during development of the met-mesencephalic region, we first compared Wnt-1 and En-2 expression in this domain by in situ hybridization in mouse embryos after embryonic day 8.5. A ring of Wnt-1-expressing cells is detected encircling the neural tube in the met-mesencephalic region at least until day 12.5. This ring consistently overlapped with the En-2 expression domain, and corresponds to the position of this latter gene's maximal expression. We subsequently studied ChickEn ectopic induction in chick embryos grafted with various portions of met-mesencephalon. When the graft originated from the level of the Wnt-1-positive ring, ChickEn induction was observed in 71% of embryos, and in these cases correlated with Wnt-1 expression in the grafted tissue. In contrast, this percentage dropped significantly when the graft was taken from more rostral or caudal parts of the mesencephalic vesicle. Taken together, these results are compatible with a prolonged role of Wnt-1 in the specification and/or development of the met-mesencephalic region, and show that Wnt-1 could be directly or indirectly involved in the regulation of En-2 expression around the Wnt-1-positive ring during this time. We also provide data on the position of the Wnt-1-positive ring relative to anatomical boundaries in the neural tube, which suggest a more general role for the Wnt-1 protein as a positional signal involved in organizing the met-mesencephalic domain.

Developmentally regulated expression of alpha 6 integrin in avian embryos

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 197-211 ◽  
Author(s):  
M. Bronner-Fraser ◽  
M. Artinger ◽  
J. Muschler ◽  
A.F. Horwitz
Keyword(s):  
Nervous System ◽  
Neural Tube ◽  
Integrin Subunit ◽  
Developmentally Regulated ◽  
Commissural Neurons ◽  
Regulated Expression ◽  
Neuroepithelial Cells ◽  
Beta 1 Integrin ◽  
Intense Immunoreactivity ◽  
Developing Nervous System

The distribution pattern of the avian alpha 6 integrin subunit was examined during early stages of development. The results show that this subunit is prevalent in cells of the developing nervous system and muscle. alpha 6 is first observed on neuroepithelial cells of the cranial neural plate and trunk neural tube. With time, immunoreactivity becomes prominent near the lumen and ventrolateral portions of the neural tube, co-distributing with neurons and axons, particularly notable on commissural neurons. The alpha 6 expression pattern is dynamic in the neural tube, with immunoreactivity peaking by embryonic day 6 (stage 30) and decreasing thereafter. The ventral roots and retina exhibit high levels of immunoreactivity throughout development. In the peripheral nervous system, alpha 6 immunoreactivity first appears on a subpopulation of sympathoadrenal cells around the dorsal aorta and later in the dorsal root ganglia shortly after gangliogenesis. Immunoreactivity appears on prospective myotomal cells as the somites delaminate into the dermomyotome and sclerotome, remaining prominent on myoblasts and differentiated muscle at all stages. The mesonephros also has intense immunoreactivity. In the periphery, alpha 6 immunoreactive regions often in proximity to laminin, which is thought to be the ligand of alpha 6 beta 1 integrin.

Effects of Levetiracetam on neural tube development and closure of the chick embryos in ovo

2012 ◽  
Vol 28 (7) ◽  
pp. 969-976 ◽  
Author(s):  
Füsun Demirçivi Özer ◽  
Adıgüzel Demirel ◽  
Özlem Yılmaz Dilsiz ◽  
Murat Aydın ◽  
Nail Özdemir ◽  
...  
Keyword(s):  
Neural Tube ◽  
Chick Embryos ◽  
In Ovo ◽  
Neural Tube Development

Spinal congenital dermal sinus in a chick embryo model

2009 ◽  
Vol 3 (1) ◽  
pp. 24-28 ◽  
Author(s):  
Jasper van Aalst ◽  
Toon F. M. Boselie ◽  
Emile A. M. Beuls ◽  
Johan S. H. Vles ◽  
Henny W. M. van Straaten
Keyword(s):  
Experimental Study ◽  
Animal Model ◽  
Neural Tube ◽  
Split Cord Malformation ◽  
Dermal Sinus ◽  
Chick Embryos ◽  
In Ovo ◽  
Surface Ectoderm ◽  
Chick Embryo Model ◽  
Congenital Dermal Sinus

Object The origin of spinal congenital dermal sinuses is not known. A local nondisjunction of the closing neural tube and the epidermal ectoderm is thought to be the cause of this malformation. In this experimental study, a nondisjunction was mimicked in chick embryos to create an animal model for the dermal sinus. Methods A piece of amniotic tissue was implanted in the closing neural tube in ovo in chick embryos at 2 days of incubation. A total of 50 embryos were manipulated. After a further incubation time of 2–7 days, the embryos were macroscopically and histologically evaluated. Results Dermal sinus–like anomalies were induced in 24 embryos. The induced abnormalities varied from superficial, epidermal lesions to epidermal dimples continuing as a strand of tissue toward the neural tube. This strand invariably was of nonneuronal origin. Additionally, in 3 embryos a split cord malformation was noted, most likely caused by damage to the neural tube during implantation. Conclusions Implantation of donor amniotic tissue in the closing chick neural tube does result in a dimple, from which a strand of tissue continues to the neural tube in various cases, indicating that formation of a dermal sinus–like anomaly can be successfully induced by experimental continuation of the connection between neural tube and surface ectoderm. This finding strengthens the hypothesis that a human dermal sinus arises after nondisjunction of neural tube and surface ectoderm.

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