Talk:Neural Crest - Peripheral Nervous System
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Cite this page: Hill, M.A. (2024, April 27) Embryology Neural Crest - Peripheral Nervous System. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_Crest_-_Peripheral_Nervous_System |
2016
Neuronal differentiation in the developing human spinal ganglia
Anat Rec (Hoboken). 2016 May 25. doi: 10.1002/ar.23376. [Epub ahead of print]
Vukojevic K1, Filipovic N1, Tica Sedlar I1,2, Restovic I3, Bocina I4, Pintaric I1, Saraga-Babic M1.
Abstract
The spatiotemporal developmental pattern of the neural crest cells differentiation towards the first appearance of the neuronal subtypes was investigated in developing human spinal ganglia between the 5th -10th developmental week using immunohistochemistry and immunofluorescence methods. First NF200 (neurofilament-200, likely-myelinated mechanoreceptors) and isolectin-B4 positive neurons (likely-unmyelinated nociceptors) appeared already in the 5/6th developmental week and their number subsequently increased during progression of development. Proportion of NF200 positive cells was higher in the ventral parts of the spinal ganglia than in the dorsal parts, particularly during the 5/6th and 9/10th developmental weeks (Mann-Whitney, p=0.040 and p=0.003). NF200 and IB4 co-localized during the whole investigated period. Calcitonin gene-related peptide (CGRP, nociceptive responses), vanilloid-receptor-1 (VR1, polymodal nociceptors) and calretinin (calcium signalling) cell immunoreactivity first appeared in the 6th and 8th week, respectively, especially in the dorsal parts of the spinal ganglia. VR1 and CGRP co-localized with NF00 during the whole investigated period. Our results indicate the high potential of early differentiated neuronal cells, which slightly decreased with progression of spinal ganglia differentiation. On the contrary, the number of neuronal subtypes displayed increasing differentiation at later developmental stage. The great diversity of phenotypic expression found in the spinal ganglia neurons is the result of a wide variety of influences, occurring at different stages of development in a large potential repertory of these neurons. Understanding the pathway of neural differentiation in the human spinal ganglia could be important for the studies dealing with process of regeneration of damaged spinal nerves or during repair of pathological changes within affected ganglia. This article is protected by copyright. All rights reserved. © 2016 Wiley Periodicals, Inc. KEYWORDS: CGRP; IB4; NF200; VR1; human embryo; spinal ganglia PMID 27225905
2011
Npn-1 contributes to axon-axon interactions that differentially control sensory and motor innervation of the limb
PLoS Biol. 2011 Feb;9(2):e1001020. Epub 2011 Feb 22.
Huettl RE, Soellner H, Bianchi E, Novitch BG, Huber AB. Source Institute of Developmental Genetics, Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg, Germany.
Abstract
The initiation, execution, and completion of complex locomotor behaviors are depending on precisely integrated neural circuitries consisting of motor pathways that activate muscles in the extremities and sensory afferents that deliver feedback to motoneurons. These projections form in tight temporal and spatial vicinities during development, yet the molecular mechanisms and cues coordinating these processes are not well understood. Using cell-type specific ablation of the axon guidance receptor Neuropilin-1 (Npn-1) in spinal motoneurons or in sensory neurons in the dorsal root ganglia (DRG), we have explored the contribution of this signaling pathway to correct innervation of the limb. We show that Npn-1 controls the fasciculation of both projections and mediates inter-axonal communication. Removal of Npn-1 from sensory neurons results in defasciculation of sensory axons and, surprisingly, also of motor axons. In addition, the tight coupling between these two heterotypic axonal populations is lifted with sensory fibers now leading the spinal nerve projection. These findings are corroborated by partial genetic elimination of sensory neurons, which causes defasciculation of motor projections to the limb. Deletion of Npn-1 from motoneurons leads to severe defasciculation of motor axons in the distal limb and dorsal-ventral pathfinding errors, while outgrowth and fasciculation of sensory trajectories into the limb remain unaffected. Genetic elimination of motoneurons, however, revealed that sensory axons need only minimal scaffolding by motor axons to establish their projections in the distal limb. Thus, motor and sensory axons are mutually dependent on each other for the generation of their trajectories and interact in part through Npn-1-mediated fasciculation before and within the plexus region of the limbs.
PMID: 21364975
http://www.ncbi.nlm.nih.gov/pubmed/21364975
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001020
