scholarly journals Solitary aortic arch artery. A result of surgical ablation of cardiac neural crest and nodose placode in the avian embryo.

Circulation ◽  
1989 ◽  
Vol 80 (5) ◽  
pp. 1469-1475 ◽  
Author(s):  
T H Rosenquist ◽  
M L Kirby ◽  
L H van Mierop
Keyword(s):  
Neural Crest ◽  
Aortic Arch ◽  
Avian Embryo ◽  
Surgical Ablation ◽  
Cardiac Neural Crest ◽  
Nodose Placode

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.

Abnormal histology of the aortic arch in coarctation of the aorta

1993 ◽  
Vol 3 (4) ◽  
pp. 412-416 ◽  
Author(s):  
Derk W. Wolterbeek ◽  
Arie P. Kappetein ◽  
Adriana C. Gittenberger–de Groot
Keyword(s):  
Neural Crest ◽  
Aortic Arch ◽  
Aortic Coarctation ◽  
Coarctation Of The Aorta ◽  
Lower Number ◽  
Descending Aorta ◽  
Aortic Isthmus ◽  
Cardiac Neural Crest ◽  
The Media

SummaryWe examined the number of elastic lamellae in the wall of the proximal aortic arch, aortic isthmus and descending aorta in patients with coarctation of the aorta. In the proximal aortic arch, the number of elastic lamellae was significantly lower in patients with coarctation compared to those with normal hearts without aortic anomalies and those with intracardiac defects but without aortic anomalies. The isthmus also showed a significantly lower number of elastic lamellae in the presence of preductal coarctation. In the descending aorta, the number of elastic lamellae was not significantly different between the different groups. There is doubt about the etiology of coarctation. Recent investigations showed that cells from the cardiac neural crest contribute to the formation of the arch arteries and the media of the arch. A developmental error of the neural crest might be responsible for the abnormal mural structures found in patients with aortic coarctation.

L-type Ca2+ channel function in the avian embryonic heart after cardiac neural crest ablation

2005 ◽  
Vol 288 (3) ◽  
pp. H1173-H1178 ◽  
Author(s):  
Carol A. Nichols ◽  
Tony L. Creazzo
Keyword(s):  
Neural Crest ◽  
Single Channel ◽  
Persistent Truncus Arteriosus ◽  
Surgical Ablation ◽  
Time Frequency ◽  
Cardiac Neural Crest ◽  
Channel Function ◽  
Open Time ◽  
Mammalian Embryos ◽  
The Mean

In avian and mammalian embryos, surgical ablation or severely reduced migration of the cardiac neural crest leads to a failure of outflow tract septation known as persistent truncus arteriosus (PTA) and leads to embryo lethality due partly to impaired excitation-contraction coupling stemming primarily from a reduction in the L-type Ca2+ current ( ICa,L). Decreased ICa,L occurs without a corresponding reduction in the α1-subunit of the Ca2+ channel. We hypothesize that decreased ICa,L is due to reduced function at the single channel level. The cell-attached patch clamp with Na+ as the charge carrier was used to examine single Ca2+ channel activity in myocytes from normal hearts from sham-operated embryos and from hearts diagnosed with PTA at embryonic days (ED) 11 and 15 after laser ablation of the cardiac neural crest. In normal hearts, the number of single channel events per 200-ms depolarization and the mean open channel probability ( Po) was 1.89 ± 0.17 and 0.067 ± 0.008 for ED11 and 1.14 ± 0.17 and 0.044 ± 0.005 for ED15, respectively. These values represent a normal reduction in channel function and ICa,L observed with development. However, the number of single channel events was significantly reduced in hearts with PTA at both ED11 and ED15 (71% and 47%, respectively) with a corresponding reduction in Po (75% and 43%). The open time frequency histograms were best fitted by single exponentials with similar decay constants (τ ≅ 4.5 ms) except for the sham operated at ED15 (τ = 3.4 ms). These results indicate that the cardiac neural crest influences the development of myocardial Ca2+ channels.

scholarly journals Effects of the size of lesions of the cardiac neural crest at various embryonic ages on incidence and type of cardiac defects.

Circulation ◽  
1986 ◽  
Vol 73 (2) ◽  
pp. 360-364 ◽  
Author(s):  
W T Besson ◽  
M L Kirby ◽  
L H Van Mierop ◽  
J R Teabeaut
Keyword(s):  
Neural Crest ◽  
Cardiac Defects ◽  
Cardiac Neural Crest

The cephalic neural crest provides pericytes and smooth muscle cells to all blood vessels of the face and forebrain

Development ◽  
2001 ◽  
Vol 128 (7) ◽  
pp. 1059-1068 ◽  
Author(s):  
H.C. Etchevers ◽  
C. Vincent ◽  
N.M. Le Douarin ◽  
G.F. Couly
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Neural Crest ◽  
Muscle Cells ◽  
Embryonic Cell ◽  
Avian Embryo ◽  
Connective Tissues ◽  
The Face ◽  
Mesodermal Origin ◽  
The Central Nervous System

Most connective tissues in the head develop from neural crest cells (NCCs), an embryonic cell population present only in vertebrates. We show that NCC-derived pericytes and smooth muscle cells are distributed in a sharply circumscribed sector of the vasculature of the avian embryo. As NCCs detach from the neural folds that correspond to the future posterior diencephalon, mesencephalon and rhombencephalon, they migrate between the ectoderm and the neuroepithelium into the anterior/ventral head, encountering mesoderm-derived endothelial precursors. Together, these two cell populations build a vascular tree rooted at the departure of the aorta from the heart and ramified into the capillary plexi that irrigate the forebrain meninges, retinal choroids and all facial structures, before returning to the heart. NCCs ensheath each aortic arch-derived vessel, providing every component except the endothelial cells. Within the meninges, capillaries with pericytes of diencephalic and mesencephalic neural fold origin supply the forebrain, while capillaries with pericytes of mesodermal origin supply the rest of the central nervous system, in a mutually exclusive manner. The two types of head vasculature contact at a few defined points, including the anastomotic vessels of the circle of Willis, immediately ventral to the forebrain/midbrain boundary. Over the course of evolution, the vertebrate subphylum may have exploited the exceptionally broad range of developmental potentialities and the plasticity of NCCs in head remodelling that resulted in the growth of the forebrain.

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