Apparatus and Current Techniques in the Preparation of Avian Embryos for Microsurgery and for Observing Embryonic Behavior
About: This article is published in BioScience.The article was published on 1970-08-01. It has received 69 citations till now.
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TL;DR: The method of embryonic tissue transplantation was used to confirm the dual origin of avian cranial sensory ganglia, to map precise locations of the anlagen of these sensory neurons, and to identify placodal and neural crest-derived neurons within ganglia.
Abstract: The method of embryonic tissue transplantation was used to confirm the dual origin of avian cranial sensory ganglia, to map precise locations of the anlagen of these sensory neurons, and to identify placodal and neural crest-derived neurons within ganglia. Segments of neural crest or strips of presumptive placodal ectoderm were excised from chick embryos and replaced with homologous tissues from quail embryos, whose cells contain a heterochromatin marker. Placode-derived neurons associated with cranial nerves V, VII, IX, and X are located distal to crest-derived neurons. The generally larger, embryonic placodal neurons are found in the distal portions of both lobes of the trigeminal ganglion, and in the geniculate, petrosal and nodose ganglia. Crest-derived neurons are found in the proximal trigeminal ganglion and in the combined proximal ganglion of cranial nerves IX and X. Neurons in the vestibular and acoustic ganglia of cranial nerve VIII derive from placodal ectoderm with the exception of a few neural crest-derived neurons localized to regions within the vestibular ganglion. Schwann sheath cells and satellite cells associated with all these ganglia originate from neural crest. The ganglionic anlagen are arranged in cranial to caudal sequence from the level of the mesencephalon through the third somite. Presumptive placodal ectoderm for the VIIIth, the Vth, and the VIIth, IXth, and Xth ganglia are located in a medial to lateral fashion during early stages of development reflecting, respectively, the dorsolateral, intermediate, and epibranchial positions of these neurogenic placodes.
653 citations
TL;DR: To follow the early migratory behavior of avian cephalic neural crest cells, neural fold tissue was transplanted orthotopically from a 3 H-thymidine-labeled donor into an unlabeled host and the embryos were indistinguishable from those which had received orthotopic transplants.
458 citations
TL;DR: 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, 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.
415 citations
TL;DR: The present study defined more precisely the regions of premigratory cranial neural crest which are needed for normal conotruncal development and ablated various regions and lengths using microcautery.
Abstract: Neural crest cells from the cranial region of the neural fold populate the outflow tract of the developing chick heart. Removal of this region of premigratory neural crest has been shown previously to result in a high percentage of conotruncal malformations. The present study was undertaken to define more precisely the regions of premigratory neural crest which are needed for normal conotruncal development. Various regions and lengths of premigratory cranial neural crest were ablated using microcautery. Three defects in conotruncal development were significantly correlated with the neural crest ablation. These were high ventricular septal defect, single outflow vessel originating from the right ventricle, and single outflow vessel overriding the ventricular septum.
278 citations
TL;DR: It is speculated that PTA is a direct result of the decreased population of mesenchymal cells derived from the arch 3 through 6 neural crest regions, and may be related to altered hemodynamics due to anomalies induced by neural crest ablation.
Abstract: To investigate the contribution of cranial neural crest cells to the developing cardiovascular system in the chick embryo, cauterization of various regions of cranial neural crest was performed. Five regions may be distinguished, each of which contributes mesenchyme to pharyngeal (branchial) arches 1 through 4 and 6. Ablation of arch 3, 4, and 6 regions resulted in a high incidence of persistent truncus arteriosus (PTA) associated with anomalies of the aortic arch. Dextroposed aorta (DPA) or anomalies of the inflow tract were found in all ablation groups. Although anomalies of the aortic arch arteries were induced in all ablation groups and were usually associated with intracardiac anomalies, those of the third and right fourth aortic arch were most frequent in the arch 4 and arch 4 + 6 groups. Anomalies of the sixth aortic arch were most frequent after extensive ablations that included the arch 6 region. We speculate that PTA is a direct result of the decreased population of mesenchymal cells derived from the arch 3 through 6 neural crest regions. DPA or anomalies of the inflow tract may be related to altered hemodynamics due to anomalies induced by neural crest ablation. Anomalies of the aortic arch arteries may be caused by either the direct or indirect process.
252 citations
References
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TL;DR: The failure to perform the integrated prehatching and hatching behavior may be due to either one of the following causes: (1)Absence of specific sensory information; (2) Absence of non-specific excitatory stimulation reducing muscle tonus; (3) Transneuronal degeneration in trigeminal medullary or in higher centers; (4) Damage in the midbrain and/or cerebellum.
Abstract: The neural crest and placodal primordia of the trigeminal ganglion were extirpated bilaterally at stages 11–12. Tests of the tactile sensitivity of different head regions showed the absence of responses to stimulation in 31 of 35 deafferented embryos. In a histological study of eight randomly selected experimental embryos small residual ganglia and trigeminal nerves were found; however, they were apparently functionally ineffective. Midbrain and cerebellar defects were found in 60% of the embryos.
Periodic motility was recorded mechanically, as in previous studies, in embryos between 9 and 17 days. Random motility up to 15 days was not different in normal and deafferented embryos. This implies that self-stimulation of the head, for instance, by brushing of legs or wings against the head, or proprioceptive self-stimulation, play no role in the random motility at least up to 15 days. A decline of spontaneous motility which occurs in normal embryos after 17 days, begins in experimental embryos already at 15 days. This may be due to the absence of sensory input or, at least in the majority of cases, to the above-metioned brain damage.
The operated embryos did not hatch but remained in a position characteristic of the 17-day stage. The failure to perform the integrated prehatching and hatching behavior may be due to either one of the following causes: (1) Absence of specific sensory information; (2) Absence of non-specific excitatory stimulation reducing muscle tonus; (3) Transneuronal degeneration in trigeminal medullary or in higher centers; (4) Damage in the midbrain and/or cerebellum.
36 citations
TL;DR: Using microsurgical techniques spinal “gaps” were made in the thoracic level of chick embryos at two days of incubation by removing small lengths of neural tissue, and three of the spinal embryos which were artificially hatched were not able to stand or walk after two days.
Abstract: Using microsurgical techniques spinal “gaps” were made in the thoracic level of chick embryos at two days of incubation by removing small lengths of neural tissue. These same embryos were then examined in detail between 17 days and hatching for any behavioral modifications.
The frequency and patterns of various movements anterior to the gap were found to be similar to control embryos. Leg movements were also found to be equal in number to those of the controls. Operated embryos, while being able to orient correctly in the egg and to pip the shell, were not able to hatch on their own. This was due to an inability of these embryos to coordinate movements of the legs with movements anterior to the spinal gap, and to the absence of vigorous stemming movements of the legs against the shell. This prohibited them from cracking and rotating around the sell and hence from hatching.
Three of the spinal embryos which were artificially hatched (pulled out of shell) were not able to stand or walk after two days. However, the legs of these chicks did show “spontaneous” alternating kicking movements and were responsive to stimulation.
30 citations
25 citations
TL;DR: A comparison of the qualitative aspects of prehatching behavior showed an increase of head movements in embryos without the right wing, which was strikingly similar to embryos with both wings intact.
Abstract: The right wing of chick embryos, stages 17–18, was extirpated with a view to study the effect of the absence of the right wing on prehatching motility and hatching behavior. Half of the embryos which survived, hatched normally. Detailed observations on these embryos showed that they followed the typical sequence of behaviorial events from day 17 until hatching. The types of behavior patterns were strikingly similar to embryos with both wings intact. A comparison of the qualitative aspects of prehatching behavior showed an increase of head movements in embryos without the right wing.
17 citations