scholarly journals Notochord grafts do not suppress formation of neural crest cells or commissural neurons

Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 877-886 ◽  
Author(s):  
K.B. Artinger ◽  
M. Bronner-Fraser

Grafting experiments previously have established that the notochord affects dorsoventral polarity of the neural tube by inducing the formation of ventral structures such as motor neurons and the floor plate. Here, we examine if the notochord inhibits formation of dorsal structures by grafting a notochord within or adjacent to the dorsal neural tube prior to or shortly after tube closure. In all cases, neural crest cells emigrated from the neural tube adjacent to the ectopic notochord. When analyzed at stages after ganglion formation, the dorsal root ganglia appeared reduced in size and shifted in position in embryos receiving grafts. Another dorsal cell type, commissural neurons, identified by CRABP and neurofilament immunoreactivity, differentiated in the vicinity of the ectopic notochord. Numerous neuronal cell bodies and axonal processes were observed within the induced, but not endogenous, floor plate 1 to 2 days after implantation but appeared to be cleared with time. These results suggest that dorsally implanted notochords cannot prevent the formation of neural crest cells or commissural neurons, but can alter the size and position of neural crest-derived dorsal root ganglia.

Development ◽  
1989 ◽  
Vol 106 (1) ◽  
pp. 85-93 ◽  
Author(s):  
C. Kalcheim ◽  
M.A. Teillet

We have investigated dorsal root ganglion formation, in the avian embryo, as a function of the composition of the paraxial somitic mesoderm. Three or four contiguous young somites were unilaterally removed from chick embryos and replaced by multiple cranial or caudal half-somites from quail embryos. Migration of neural crest cells and formation of DRG were subsequently visualized both by the HNK-1 antibody and the Feulgen nuclear stain. At advanced migratory stages (as defined by Teillet et al. Devl Biol. 120, 329–347 1987), neural crest cells apposed to the dorsolateral faces of the neural tube were distributed in a continuous, nonsegmented pattern that was indistinguishable on unoperated sides and on sides into which either half of the somites had been grafted. In contrast, ventrolaterally, neural crest cells were distributed segmentally close to the neural tube and within the cranial part of each normal sclerotome, whereas they displayed a nonsegmental distribution when the graft involved multiple cranial half-somites or were virtually absent when multiple caudal half-somites had been implanted. In spite of the identical dorsal distribution of neural crest cells in all embryos, profound differences in the size and segmentation of DRG were observed during gangliogenesis (E4–9) according to the type of graft that had been performed. Thus when the implant consisted of compound cranial half-somites, giant, coalesced ganglia developed, encompassing the entire length of the graft. On the other hand, very small, dorsally located ganglia with irregular segmentation were seen at the level corresponding to the graft of multiple caudal half-somites. We conclude that normal morphogenesis of dorsal root ganglia depends upon the craniocaudal integrity of the somites.


Development ◽  
1993 ◽  
Vol 119 (4) ◽  
pp. 1217-1228 ◽  
Author(s):  
R.M. Campbell ◽  
A.C. Peterson

The floor plate is situated at the ventral midline of the neural tube and is an important intermediate target for commissural axons. During elongation, these axons converge bilaterally on the ventral midline neural tube and after crossing the floor plate make an abrupt rostral turn. Ample evidence indicates that the initial projection of commissural axons to the floor plate is guided by a chemotropic factor secreted by floor plate cells. However, the way in which the subsequent interaction of these axons with the floor plate leads them to make further trajectory changes remains undefined. In an effort to gain further understanding of the structure and function of floor plate cells, we have taken advantage of a line of transgenic mice in which these cells express beta-galactosidase and thus can be stained by histochemical means. In this line, a genomic imprinting mechanism restricts the expression of the lacZ transgene to only a proportion of the floor plate cells, allowing their morphology to be appreciated with particular clarity. Our analysis revealed that the basal processes of floor plate cells are flattened in their rostrocaudal dimension and possess fine lateral branches which are aligned with commissural axons. Unexpectedly, beta-galactosidase activity was also detected within longer transverse linear profiles traversing the floor plate whose ultrastructural appearance was not that of floor plate cells but instead corresponded to that of commissural axons. Enzyme activity was not detected in more proximal axonal segments or in the neuronal cell bodies from which these axons originated. Therefore, we propose that the transgene product, and potentially other proteins synthesized by floor plate cells, can be transferred to decussating axons.


Development ◽  
1991 ◽  
Vol 113 (1) ◽  
pp. 207-216 ◽  
Author(s):  
C.D. Stern ◽  
K.B. Artinger ◽  
M. Bronner-Fraser

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.


Development ◽  
2000 ◽  
Vol 127 (13) ◽  
pp. 2811-2821 ◽  
Author(s):  
Y. Wakamatsu ◽  
T.M. Maynard ◽  
J.A. Weston

Avian trunk neural crest cells give rise to a variety of cell types including neurons and satellite glial cells in peripheral ganglia. It is widely assumed that crest cell fate is regulated by environmental cues from surrounding embryonic tissues. However, it is not clear how such environmental cues could cause both neurons and glial cells to differentiate from crest-derived precursors in the same ganglionic locations. To elucidate this issue, we have examined expression and function of components of the NOTCH signaling pathway in early crest cells and in avian dorsal root ganglia. We have found that Delta1, which encodes a NOTCH ligand, is expressed in early crest-derived neuronal cells, and that NOTCH1 activation in crest cells prevents neuronal differentiation and permits glial differentiation in vitro. We also found that NUMB, a NOTCH antagonist, is asymmetrically segregated when some undifferentiated crest-derived cells in nascent dorsal root ganglia undergo mitosis. We conclude that neuron-glia fate determination of crest cells is regulated, at least in part, by NOTCH-mediated lateral inhibition among crest-derived cells, and by asymmetric cell division.


2020 ◽  
Vol 21 (11) ◽  
pp. 3839 ◽  
Author(s):  
Kevin Glaesel ◽  
Caroline May ◽  
Katrin Marcus ◽  
Veronika Matschke ◽  
Carsten Theiss ◽  
...  

The wide-ranging influence of vascular endothelial growth factor (VEGF) within the central (CNS) and peripheral nervous system (PNS), for example through effects on axonal growth or neuronal cell survival, is mainly mediated by VEGF receptor 2 (VEGFR-2). However, the regulation of VEGFR-2 expression during development is not yet well understood. As microRNAs are considered to be key players during neuronal maturation and regenerative processes, we identified the two microRNAs (miRNAs)—miR-129-5p and miR-130a-3p—that may have an impact on VEGFR-2 expression in young and mature sensory and lower motor neurons. The expression level of VEGFR-2 was analyzed by using in situ hybridization, RT-qPCR, Western blot, and immunohistochemistry in developing rats. microRNAs were validated within the spinal cord and dorsal root ganglia. To unveil the molecular impact of our candidate microRNAs, dissociated cell cultures of sensory and lower motor neurons were transfected with mimics and inhibitors. We depicted age-dependent VEGFR-2 expression in sensory and lower motor neurons. In detail, in lower motor neurons, VEGFR-2 expression was significantly reduced during maturation, in conjunction with an increased level of miR-129-5p. In sensory dorsal root ganglia, VEGFR-2 expression increased during maturation and was accompanied by an overexpression of miR-130a-3p. In a second step, the functional significance of these microRNAs with respect to VEGFR-2 expression was proven. Whereas miR-129-5p seems to decrease VEGFR-2 expression in a direct manner in the CNS, miR-130a-3p might indirectly control VEGFR-2 expression in the PNS. A detailed understanding of genetic VEGFR-2 expression control might promote new strategies for the treatment of severe neurological diseases like ischemia or peripheral nerve injury.


2008 ◽  
Vol 125 (11-12) ◽  
pp. 1033-1047 ◽  
Author(s):  
Judy Bononi ◽  
Angela Cole ◽  
Paul Tewson ◽  
Andrew Schumacher ◽  
Roger Bradley

2004 ◽  
Vol 1 (1) ◽  
pp. 85-93 ◽  
Author(s):  
ÅSA FEX SVENNINGSEN ◽  
DAVID R. COLMAN ◽  
LILIANA PEDRAZA

The evolutionary origin of myelinating cells in the vertebrate nervous system remains a mystery. A clear delineation of the developmental potentialities of neuronal support cells in the CNS and PNS might aid in formulating a hypothesis about the origins of myelinating cells. Although a glial-precursor cell in the CNS can differentiate into oligodendrocytes (OLs), Schwann cells (SCs) and astrocytes, a homologous multipotential cell has not yet been found in the PNS. Here, we identify a cell type of embryonic dorsal root ganglia (DRG) of the PNS – the satellite cell – that develops into OLs, SCs and astrocytes. Interestingly, satellite-cell-derived OL precursors were found in cultures prepared from embryonic day 17 (E17) to postnatal day 8 (P8) ganglia, but not from adult DRGs, revealing a narrow developmental window for multipotentiality. We suggest that compromising the organization of the ganglia triggers a differentiation pathway in a subpopulation of satellite cells, inducing them to become myelinating cells with either a CNS or PNS phenotype. Our data provide an additional, novel piece in the myelinating-cell-precursor puzzle, and lead to the concept that cells in the CNS and PNS that function to ensheath neuronal cell bodies and axons can differentiate into OLs, SCs and astrocytes. In sum, it appears that glial fate might be determined over and above the CNS/PNS dichotomy. Last, we suggest that primordial ensheathing cells form the original cell population in which the myelination program first evolved.


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