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Original Paper

Migration of Enteric Neural Crest Cells in Relation to Growth of the Gut in Avian Embryos

Newgreen D.F.a · Southwell B.b · Hartley L.c · Allan I.J.d,†

Author affiliations

aThe Murdoch Institute for Research into Birth Defects, Royal Children’s Hospital, bDepartment of Anatomy and Cell Biology, University of Melbourne, cWalter and Eliza Hall Institute, and dDepartment of Zoology, University of Melbourne, Parkville, Melbourne, Viet., Australia

Related Articles for ""

Acta Anatomica 1996;157:105–115

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: August 31, 1996
Accepted: January 06, 1997
Published online: July 17, 2008
Issue release date: 1996

Number of Print Pages: 11
Number of Figures: 0
Number of Tables: 0

ISSN: 1422-6405 (Print)
eISSN: 1422-6421 (Online)

For additional information: https://www.karger.com/CTO

Abstract

Neural crest cell migration in the gut and the growth of the mid- and hindgut of avian embryos was investigated by a combination of whole-mount immunofluorescence of the HNK-1 neural crest marker epitope, chorioallantoic membrane grafting and morphometry. HNK-1-labelled cells advanced rostrocaudally in the gut of quail embryos (to the duodenum by stage HH 21 to the umbilicus by HH 25, to the ceca by HH 27, to the cloaca by HH 33). The timetable in chick embryos appeared to be slightly slower, but neural cells were obscured by background fluorescence in this species. More rostral regions of the gut commenced rapid growth earlier than more caudal regions (preumbilical small intestine after HH 26, postumbilical small intestine after HH 27 and colorectum after HH 28), and the small intestine and ceca grew most rapidly in length while the colorectum grew most rapidly in diameter. The rates of growth of the gut were low prior to the stage when HNK-1-labelled cells normally arrive in the small intestine, ceca and rostral colorectum, but increased dramatically after arrival. In the caudal colorectum rapid growth had commenced at the time of arrival of these cells. These data are consistent with the idea that a delay in arrival of vagal neural crest cells at any point in the intestine could jeopardize the ability of the cells to fully populate the remainder of the gut, due to the normal growth spurt causing the migration end-point to recede faster than the rate of neural crest cell migration. Thus, a mismatch in timing of neural crest cell migration and gut growth could play a role in the etiology of some forms of Hirschsprung’s disease.

© 1996 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: August 31, 1996
Accepted: January 06, 1997
Published online: July 17, 2008
Issue release date: 1996

Number of Print Pages: 11
Number of Figures: 0
Number of Tables: 0

ISSN: 1422-6405 (Print)
eISSN: 1422-6421 (Online)

For additional information: https://www.karger.com/CTO


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