Talk:Neural Crest - Enteric Nervous System

About Discussion Pages

On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, May 7) Embryology Neural Crest - Enteric Nervous System. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_Crest_-_Enteric_Nervous_System

10 Most Recent

Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)

Enteric Nervous System Development

<pubmed limit=5>Enteric Nervous System Developmentpubmed>

Enteric Nervous System Development Abnormalities

<pubmed limit=5>Enteric Nervous System Development Abnormalities</pubmed>

2013

Development and developmental disorders of the enteric nervous system

Nat Rev Gastroenterol Hepatol. 2013 Jan;10(1):43-57. doi: 10.1038/nrgastro.2012.234. Epub 2012 Dec 11.

Obermayr F, Hotta R, Enomoto H, Young HM. Source Department of Pediatric Surgery, University Children's Hospital, University of Tübingen, Hoppe-Seyler Straße 3, Tübingen 72076, Germany.

Abstract

The enteric nervous system (ENS) arises from neural crest-derived cells that migrate into and along the gut, leading to the formation of a complex network of neurons and glial cells that regulates motility, secretion and blood flow. This Review summarizes the progress made in the past 5 years in our understanding of ENS development, including the migratory pathways of neural crest-derived cells as they colonize the gut. The importance of interactions between neural crest-derived cells, between signalling pathways and between developmental processes (such as proliferation and migration) in ensuring the correct development of the ENS is also presented. The signalling pathways involved in ENS development that were determined using animal models are also described, as is the evidence for the involvement of the genes encoding these molecules in Hirschsprung disease-the best characterized paediatric enteric neuropathy. Finally, the aetiology and treatment of Hirschsprung disease in the clinic and the potential involvement of defects in ENS development in other paediatric motility disorders are outlined.

PMID 23229326

Enteric neurons show a primary cilium

J Cell Mol Med. 2013 Jan;17(1):147-53. doi: 10.1111/j.1582-4934.2012.01657.x. Epub 2012 Dec 4.

Luesma MJ, Cantarero I, Castiella T, Soriano M, Garcia-Verdugo JM, Junquera C. Source Department of Human Anatomy and Histology, Faculty of Medicine, University of Zaragoza, Zaragoza, Spain. mjluesma@unizar.es

Abstract

The primary cilium is a non-motile cilium whose structure is 9+0. It is involved in co-ordinating cellular signal transduction pathways, developmental processes and tissue homeostasis. Defects in the structure or function of the primary cilium underlie numerous human diseases, collectively termed ciliopathies. The presence of single cilia in the central nervous system (CNS) is well documented, including some choroid plexus cells, neural stem cells, neurons and astrocytes, but the presence of primary cilia in differentiated neurons of the enteric nervous system (ENS) has not yet been described in mammals to the best of our knowledge. The enteric nervous system closely resembles the central nervous system. In fact, the ultrastructure of the ENS is more similar to the CNS ultrastructure than to the rest of the peripheral nervous system. This research work describes for the first time the ultrastructural characteristics of the single cilium in neurons of rat duodenum myenteric plexus, and reviews the cilium function in the CNS to propose the possible role of cilia in the ENS cells. © 2012 The Authors. Published by Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

PMID 23205631

Balancing on the crest - Evidence for disruption of the enteric ganglia via inappropriate lineage segregation and consequences for gastrointestinal function

Dev Biol. 2013 Jan 31. pii: S0012-1606(13)00042-0. doi: 10.1016/j.ydbio.2013.01.024. [Epub ahead of print]

Musser MA, Michelle Southard-Smith E. Source Division of Genetic Medicine, Department of Medicine and the PhD Program in Human Genetics, Center for Human Genetic Research, Vanderbilt University School of Medicine, Nashville, TN, USA. Abstract Normal enteric nervous system (ENS) development relies on numerous factors, including appropriate migration, proliferation, differentiation, and maturation of neural crest (NC) derivatives. Incomplete rostral to caudal migration of enteric neural crest-derived progenitors (ENPs) down the gut is at least partially responsible for the absence of enteric ganglia that is a hallmark feature of Hirschsprung disease (HSCR). The thought that ganglia proximal to aganglionosis are normal has guided surgical procedures for HSCR patients. However, chronic gastrointestinal dysfunction suffered by a subset of patients after surgery as well as studies in HSCR mouse models suggest that aberrant NC segregation and differentiation may be occurring in ganglionated regions of the intestine. Studies in mouse models that possess enteric ganglia throughout the length of the intestine (non-HSCR) have also found that certain genetic alterations affect neural crest lineage balance and interestingly many of these mutants also have functional gastrointestinal (GI) defects. It is possible that many GI disorders can be explained in part by imbalances in NC-derived lineages. Here we review studies evaluating ENS defects in HSCR and non-HSCR mouse models, concluding with clinical implications while highlighting areas requiring further study. Copyright © 2013 Elsevier Inc. All rights reserved.

PMID 23376538

Building a brain in the gut: development of the enteric nervous system

Clin Genet. 2013 Apr;83(4):307-16. doi: 10.1111/cge.12054. Epub 2012 Nov 27.

Goldstein A, Hofstra R, Burns A. Source Department of Pediatric Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Abstract The enteric nervous system (ENS), the intrinsic innervation of the gastrointestinal tract, is an essential component of the gut neuromusculature and controls many aspects of gut function, including coordinated muscular peristalsis. The ENS is entirely derived from neural crest cells (NCC) which undergo a number of key processes, including extensive migration into and along the gut, proliferation, and differentiation into enteric neurons and glia, during embryogenesis and fetal life. These mechanisms are under the molecular control of numerous signaling pathways, transcription factors, neurotrophic factors and extracellular matrix components. Failure in these processes and consequent abnormal ENS development can result in so-called enteric neuropathies, arguably the best characterized of which is the congenital disorder Hirschsprung disease (HSCR), or aganglionic megacolon. This review focuses on the molecular and genetic factors regulating ENS development from NCC, the clinical genetics of HSCR and its associated syndromes, and recent advances aimed at improving our understanding and treatment of enteric neuropathies. © 2012 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd. PMID 23167617

2012

The enteric nervous system

Dev Biol. 2012 Jun 1;366(1):64-73. doi: 10.1016/j.ydbio.2012.01.012. Epub 2012 Jan 24.

Sasselli V, Pachnis V, Burns AJ. Source Division of Molecular Neurobiology, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK. Abstract The enteric nervous system (ENS), the intrinsic innervation of the gastrointestinal tract, consists of numerous types of neurons, and glial cells, that are distributed in two intramuscular plexuses that extend along the entire length of the gut and control co-ordinated smooth muscle contractile activity and other gut functions. All enteric neurons and glia are derived from neural crest cells (NCC). Vagal (hindbrain) level NCC provide the majority of enteric precursors along the entire length of the gut, while a lesser contribution, that is restricted to the hindgut, arises from the sacral region of the neuraxis. After leaving the dorsal neural tube NCC undergo extensive migration, proliferation, survival and differentiation in order to form a functional ENS. This article reviews the molecular mechanisms underlying these key developmental processes and highlights the major groups of molecules that affect enteric NCC proliferation and survival (Ret/Gdnf and EdnrB/Et-3 pathways, Sox10 and Phox2b transcription factors), cell migration (Ret and EdnrB signalling, semaphorin 3A, cell adhesion molecules, Rho GTPases), and the development of enteric neuronal subtypes and morphologies (Mash1, Gdnf/neurturin, BMPs, Hand2, retinoic acid). Finally, looking to the future, we discuss the need to translate the wealth of data gleaned from animal studies to the clinical area and thus better understand, and develop treatments for, congenital human diseases affecting the ENS. Copyright © 2012 Elsevier Inc. All rights reserved. PMID 22290331