Neural Crest - Enteric Nervous System

Embryology - 16 Apr 2024 Expand to Translate
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Introduction

Myenteric plexus of the gastrointestinal tract

Human embryo neural crest cells (stage 11)

The neural crest are bilaterally paired strips of cells arising in the ectoderm at the margins of the neural tube. These cells migrate to many different locations and differentiate into many cell types within the embryo. This means that many different systems (neural, skin, teeth, head, face, heart, adrenal glands, gastrointestinal tract) will also have a contribution fron the neural crest cells.

The enteric nervous system (ENS) regulates many key aspects of the gastrointestinal tract including: motility, secretion and blood flow. In the body region, neural crest cells form the entire enteric nervous system, both neurons and glia, of the gastrointestinal tract.

Neural crest cells initially migrate into the foregut splanchnic mesoderm of the developing gastrointestinal tract, these cells then migrate caudally along the gut into the midgut. A second population of sacral neural crest cells migrate to the region of the hindgut.

The two gastrointestinal plexuses are located between the longitudinal and circular smooth muscle layers (myenteric plexus, Auerbach's plexus) and in the submucosal layer (submucosal plexus, Meissner's plexus). Interstitial cells of Cajal (ICCs) within the myenteric plexus are pacemaker cells that control peristaltic contraction waves.

These projects are the sole work of undergraduate science students and may contain errors in fact or descriptions.

Historic Embryology - Neural Crest
1879 Olfactory Organ \| 1905 Cranial and Spinal Nerves \| 1908 10 mm Peripheral \| 1910 Mammal Sympathetic \| 1920 Human Sympathetic \| 1928 Cranial ganglia \| 1939 10 Somite Embryo \| 1942 Origin \| 1957 Adrenal

Intestine Development | Gastrointestinal Tract Development

Some Recent Findings

Enteric neural crest cells regulate vertebrate stomach patterning and differentiation^[1] "In vertebrates, the digestive tract develops from a uniform structure where reciprocal epithelial-mesenchymal interactions pattern this complex organ into regions with specific morphologies and functions. Concomitant with these early patterning events, the primitive GI tract is colonized by the vagal enteric neural crest cells (vENCCs), a population of cells that will give rise to the enteric nervous system (ENS), the intrinsic innervation of the GI tract. The influence of vENCCs on early patterning and differentiation of the GI tract has never been evaluated. In this study, we report that a crucial number of vENCCs is required for proper chick stomach development, patterning and differentiation." Gastrointestinal Tract - Stomach Development
Gas1 is a receptor for sonic hedgehog to repel enteric axons^[2] "The myenteric plexus of the enteric nervous system controls the movement of smooth muscles in the gastrointestinal system. They extend their axons between two peripheral smooth muscle layers to form a tubular meshwork arborizing the gut wall. How a tubular axonal meshwork becomes established without invading centrally toward the gut epithelium has not been addressed. We provide evidence here that sonic hedgehog (Shh) secreted from the gut epithelium prevents central projections of enteric axons, thereby forcing their peripheral tubular distribution. Exclusion of enteric central projections by Shh requires its binding partner growth arrest specific gene 1 (Gas1) and its signaling component smoothened (Smo) in enteric neurons."
Review - Building a brain in the gut: development of the enteric nervous system^[3] "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."
Review - Development and developmental disorders of the enteric nervous system^[4]

More recent papers
This table allows an automated computer search of the external PubMed database using the listed "Search term" text link. This search now requires a manual link as the original PubMed extension has been disabled. The displayed list of references do not reflect any editorial selection of material based on content or relevance. References also appear on this list based upon the date of the actual page viewing. References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability. More? References \| Discussion Page \| Journal Searches \| 2019 References \| 2020 References Search term: Enteric Nervous System Development <pubmed limit=5>Enteric Nervous System Development</pubmed>

Development Overview

This data below is a summary from a study of human enteric ganglia development^[5] (ages given are gestational age GA weeks)

week 7 - rostro-caudal neural crest cell colonization of the gut complete and differentiated into neurons and glia. Interstitial cells of Cajal (ICCs) localized in the ganglion plexus.
- foregut neurons and glia were aggregated into ganglion plexus (myenteric region) not in submucosa.
- hind gut neurons and glia are dispersed within the mesenchyme.
week 9 - myenteric plexus, longitudinal and circular muscle layers formed along the entire gut.
week 12 - scattered and individual neurons and glia, and small ganglion plexuses were detected in the foregut and midgut submucosa. Muscularis mucosae formed at the foregut and midgut.
week 14 - ganglion plexus seen in the hind gut submucosa. Muscularis mucosae formed at the hindgut.
week 20 - ICCs preferentially localized at the periphery of the plexus.

Mouse Model

Mouse enteric plexus GFP ^[6]

Neural Crest Migration

Abnormalities

Intestinal Aganglionosis

(intestinal aganglionosis, Hirschsprung's disease, aganglionic colon, megacolon, congenital aganglionic megacolon, congenital megacolon) A condition caused by the lack of enteric nervous system (neural ganglia) in the intestinal tract responsible for gastric motility (peristalsis). In general, its severity is dependent upon the amount of the GIT that lacks intrinsic ganglia, due to developmental lack of neural crest migration into those segments. (More? Neural Crest System - Abnormalities)

Historically, Hirschsprung's disease takes its name from Dr Harald Hirschsprung (1830-1916) a Danish pediatrician (of German extraction). In 1886, he presented at the German Society of Pediatrics conference in Berlin a case of 2 infants who died of complications of bowel obstruction (H. Hirschsprung, Stuhltragheit Neugeborener in Folge von Dilatation und Hypertrophie des Colons, Jhrb f Kinderh 27 (1888), pp. 1-7). Later autopsies identified a dilatation and hypertrophy of large intestine, and the rectum appeared normally narrow. Hirschsprung suggested that the condition was an inborn disease and named it congenital megacolon.

The first indication in newborns is an absence of the first bowel movement, other symptoms include throwing up and intestinal infections. Clinically this is detected by one or more tests (barium enema and x ray, manometry or biopsy) and can currently only be treated by surgery. A temoporary ostomy (Colostomy or Ileostomy) with a stoma is carried out prior to a more permanent pull-through surgery.


Ostomy - Aganglionic portion removed	Stoma - intestine attached to the abdomen wall

Short section of the colon without smooth muscle neural ganglia	Aganglionic segment removed	Reattachment

Australian Statistics

Hirschsprung’s disease^[7] (1.3 per 10,000 births) ICD-10 Q43.1

A condition characterised by partial or complete bowel obstruction resulting from absence of peristalsis in a segment of bowel due to an aganglionic section of the bowel.
More than two-thirds (66.7%) of the babies born with this anomaly were males.
Women aged 40 years or older had the highest rate of affected pregnancies.

Links: Gastrointestinal Tract - Intestinal Aganglionosis | Neural Crest System - Abnormalities

References

↑ <pubmed>25519241</pubmed>
↑ <pubmed>25535338</pubmed>
↑ <pubmed>23167617</pubmed>
↑ <pubmed>23229326</pubmed>
↑ <pubmed>14991401</pubmed>
↑ <pubmed>26943905</pubmed>
↑ Abeywardana S & Sullivan EA 2008. Congenital Anomalies in Australia 2002-2003. Birth anomalies series no. 3 Cat. no. PER 41. Sydney: AIHW National Perinatal Statistics Unit.

Reviews

Articles

Books

Anderson RB, Newgreen DF, Young HM. Neural Crest and the Development of the Enteric Nervous System. In: Madame Curie Bioscience Database [Internet]. Austin (TX): Landes Bioscience; 2000-. Available from: http://www.ncbi.nlm.nih.gov/books/NBK6273/

Search PubMed

Search Pubmed: Enteric Neural Development | hirschprung's disease

Search All Databases: Enteric Neural Development

Additional Images

Abdominal portion of the sympathetic system
Great plexuses of the sympathetic system
celiac ganglia with the sympathetic plexuses

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Cite this page: Hill, M.A. (2024, April 16) Embryology Neural Crest - Enteric Nervous System. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Neural_Crest_-_Enteric_Nervous_System

What Links Here?

[PMID25519241-1] <pubmed>25519241</pubmed>

[PMID25535338-2] <pubmed>25535338</pubmed>

[PMID23167617-3] <pubmed>23167617</pubmed>

[PMID23229326-4] <pubmed>23229326</pubmed>

[PMID14991401-5] <pubmed>14991401</pubmed>

[PMID26943905-6] <pubmed>26943905</pubmed>

[7] Abeywardana S & Sullivan EA 2008. Congenital Anomalies in Australia 2002-2003. Birth anomalies series no. 3 Cat. no. PER 41. Sydney: AIHW National Perinatal Statistics Unit.

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