Extracellular matrix components of the peripheral pathway of chick trigeminal axons

Moody, Sally A.; Quigg, Marks S.; Little, Charles D.

doi:10.1002/cne.902830105

Cited by 33 publications

(15 citation statements)

References 66 publications

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“…In both chick and mouse, trigeminal neurons first develop in the opV placode followed by the mmV placode, while neural crest-derived neurons differentiate at considerably later stages (Covell and Noden, 1989; d'Amico-Martel and Noden, 1980; Moody et al, 1989a; Moody et al, 1989b; Nichols, 1986; Stainier and Gilbert, 1991; Verwoerd et al, 1981). …”

Section: Origins and Derivatives Of Neurogenic Placodesmentioning

confidence: 99%

Signaling mechanisms controlling cranial placode neurogenesis and delamination

Lassiter

Stark

Zhao

et al. 2014

Developmental Biology

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The neurogenic cranial placodes are a unique transient epithelial niche of neural progenitor cells that give rise to multiple derivatives of the peripheral nervous system, particularly, the sensory neurons. Placode neurogenesis occurs throughout an extended period of time with epithelial cells continually recruited as neural progenitor cells. Sensory neuron development in the trigeminal, epibranchial, otic, and olfactory placodes coincides with detachment of these neuroblasts from the encompassing epithelial sheet, leading to delamination and ingression into the mesenchyme where they continue to differentiate as neurons. Multiple signaling pathways are known to direct placodal development. This review defines the signaling pathways working at the finite spatiotemporal period when neuronal selection within the placodes occurs, and neuroblasts concomitantly delaminate from the epithelium. Examining neurogenesis and delamination after initial placodal patterning and specification has revealed a common trend throughout the neurogenic placodes, which suggests that both activated FGF and attenuated Notch signaling activities are required for neurogenesis and changes in epithelial cell adhesion leading to delamination. We also address the varying roles of other pathways such as the Wnt and BMP signaling families during sensory neurogenesis and neuroblast delamination in the differing placodes.

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Section: Origins and Derivatives Of Neurogenic Placodesmentioning

confidence: 99%

Signaling mechanisms controlling cranial placode neurogenesis and delamination

Lassiter

Stark

Zhao

et al. 2014

Developmental Biology

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“…TUJ1 has previously been shown to be present during the final cell divisions of neuronal precursors, immediately after cell-cycle exit, and at the beginning of neuronal differentiation (39)(40)(41)(42). We double stained transverse colon sections from E16.5 WT and HM embryos for TUJ1 and Ki67, a marker of cycling cells, or used BrdU incorporation assays to evaluate the rate of proliferation ( Figure 6D).…”

Section: Loss Of Pten In Encs Leads To Hypertrophy and Hyperplasia Ofmentioning

confidence: 99%

Deletion of Pten in the mouse enteric nervous system induces ganglioneuromatosis and mimics intestinal pseudoobstruction

Puig¹,

Champeval²,

Barbara³

et al. 2009

J. Clin. Invest.

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Intestinal ganglioneuromatosis is a benign proliferation of nerve ganglion cells, nerve fibers, and supporting cells of the enteric nervous system (ENS) that can result in abnormally large enteric neuronal cells (ENCs) in the myenteric plexus and chronic intestinal pseudoobstruction (CIPO). As phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a phosphatase that is critical for controlling cell growth, proliferation, and death, we investigated the role of PTEN in the ENS by generating mice with an embryonic, ENC-selective deletion within the Pten locus. Mutant mice died 2 to 3 weeks after birth, with clinical signs of CIPO and hyperplasia and hypertrophy of ENCs resulting from increased activity of the PI3K/PTEN-AKT-S6K signaling pathway. Further analysis revealed that PTEN was only expressed in developing mouse embryonic ENCs from E15.5 and that the rate of ENC proliferation decreased once PTEN was expressed. Specific deletion of the Pten gene in ENCs therefore induced hyperplasia and hypertrophy in the later stages of embryogenesis. This phenotype was reversed by administration of a pharmacological inhibitor of AKT. In some human ganglioneuromatosis forms of CIPO, PTEN expression was found to be abnormally low and S6 phosphorylation increased. Our study thus reveals that loss of PTEN disrupts development of the ENS and identifies the PI3K/PTEN-AKT-S6K signaling pathway as a potential therapeutic target for ganglioneuromatosis forms of CIPO. IntroductionThe enteric nervous system (ENS) regulates peristalsis, secretions, blood supply, and immune responses in the intestinal tract (1). The mammalian ENS is composed of a large number of neurons and glia that are organized into enteric ganglia distributed throughout the gut wall (2). ENS cells cluster into 2 plexi: the myenteric plexus develops first and is situated between the inner circular and outer longitudinal layers of the muscularis propia; the submucosal plexus forms later during gestation and is positioned between the muscularis propia and the muscularis mucosa (3).Neural crest cells develop from the dorsal part of the neural tube of embryos. They migrate into most of the peripheral regions to produce various derivatives including skin melanocytes and the ENS. In the vagal region, the ENS progenitors, enteric neural crest-derived cells (ENCCs), and their derivatives proliferate actively to expand the relatively small pool of progenitors that invade the foregut; they thereby generate the millions of enteric neurons and glia that are present in the adult intestine (4). A fully colonized gut, with the appropriate number of neuronal and glial cells, is required for integrated peristaltic activity of the gut wall.Many pediatric consultations are due to ENS disorders resulting from a number of neurocristopathies (5). Chronic intestinal pseudoobstruction (CIPO) is a rare, severe, and disabling disorder characterized by repetitive episodes or continuous symptoms of bowel obstruction; it is associated with substantial morbidity and mortality. There ar...

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“…Presumptive Schwann cells that can synthesise laminin are followed by sensory axons in the chick embryo (Moody et al 1989). This does not apply to motor axons and may explain why the trigeminal motor nucleus did not trace until 38 somites.…”

Section: -40 Somites (E10 5-e11)mentioning

confidence: 99%

Compartmentalisation of the developing trigeminal ganglion into maxillary and mandibular divisions does not depend on target contact

Scott

Atkinson

1999

Journal of Anatomy

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During development axons contact their target tissues with phenomenal accuracy but the mechanisms that control this homing behaviour remain largely elusive. A prerequisite to the study of the factors involved in hard-wiring the nervous system during neurogenesis is an accurate calendar of developmental events. We have studied the maxillary and mandibular components of the trigeminal system to determine the stages during embryogenesis when a gross somatotopic order is first established within the trigeminal ganglion and the axons projecting to the brainstem. The retrograde transganglionic fluorescent tracers DiO and DiI were injected into the maxillary and mandibular arches or their derivatives in fixed mouse embryos staged between 13 and 40 somites (E9-E11). After 1-4 wk, the distribution of the 2 tracers was determined using confocal laser scanning microscopy. The first maxillary nerve cell bodies and their developing axons were labelled at the 30 somite stage (E10). This was 2 somite stages earlier than the mesencephalic nucleus and the ganglion cell bodies of the mandibular nerve. The gross somatotopic division of cells within the trigeminal ganglion projecting to the maxillary and mandibular targets was established by the 32 somite stage (E10). This arrangement was evident as 2 groups of cell bodies occupying adjacent but separate regions of the trigeminal ganglion. The central branches of the maxillary and mandibular cell bodies entered the metencephalon as 2 distinct bundles at the same stage. The trigeminal motor nucleus was first detected at the 38 somite stage (E10.5).Gross somatotopy in the major divisions of the trigeminal ganglion is established before outgrowing axons have contacted their peripheral target tissue at E10.5. This suggests that target tissues do not induce somatotopy.

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Extracellular matrix components of the peripheral pathway of chick trigeminal axons

Cited by 33 publications

References 66 publications

Signaling mechanisms controlling cranial placode neurogenesis and delamination

Signaling mechanisms controlling cranial placode neurogenesis and delamination

Deletion of Pten in the mouse enteric nervous system induces ganglioneuromatosis and mimics intestinal pseudoobstruction

Compartmentalisation of the developing trigeminal ganglion into maxillary and mandibular divisions does not depend on target contact

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