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Updated: May 10, 2026

Immunostaining to Visualize Murine Enteric Nervous System Development

Immunostaining to Visualize Murine Enteric Nervous System Development

Published on: April 29, 2015

Retinaldehyde dehydrogenase enzymes regulate colon enteric nervous system structure and function.

Elizabeth C Wright-Jin¹, John R Grider, Gregg Duester

¹Department of Pediatrics, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis 63110, MO, USA.

Developmental Biology

|June 29, 2013

Summary

This summary is machine-generated.

Retinaldehyde dehydrogenases (RALDH1, RALDH2, RALDH3) are crucial for enteric nervous system (ENS) development and function. Mutations in these enzymes lead to reduced neuron density and impaired colon contractility, highlighting their collective importance.

Keywords:

Enteric nervous system Intestinal motility Retinaldehyde dehydrogenase Retinoid metabolism

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Optimized Protocol for Retinal Wholemount Preparation for Imaging and Immunohistochemistry

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Published on: December 13, 2013

Area of Science:

Developmental biology
Neuroscience
Gastroenterology

Background:

The enteric nervous system (ENS) controls intestinal function and develops from neural crest precursors.
Retinoids, particularly retinoic acid (RA), are vital for ENS development, but the precise roles of RA metabolism enzymes are unclear.
RA synthesis and degradation rates directly impact RA signaling, which is essential during development.

Purpose of the Study:

To investigate the specific contributions of retinaldehyde dehydrogenase enzymes (RALDH1, RALDH2, RALDH3) to the development and function of the enteric nervous system.
To determine the impact of mutations in RALDH enzymes on ENS structure and colon motility.

Main Methods:

Analysis of whole mount preparations of adult mouse myenteric and submucosal plexus using neuronal and glial markers (NADPH diaphorase, anti-TuJ1, anti-HuC/HuD, anti-S100β).
Examination of an allelic series of mice with mutations in Raldh1, Raldh2, and Raldh3 genes.
Assessment of enteric neuron progenitor migration and colon contractility in mutant versus wild-type mice.

Main Results:

Mice with combined Raldh1, Raldh2, and Raldh3 mutations exhibited reduced colon myenteric and submucosal neuron density.
Mutant mice showed altered neuron-to-glia ratios and increased myenteric fibers per neuron.
Impaired colon contractility was observed in RALDH mutant mice compared to wild-type controls.
Enteric neuron progenitor migration was not defective and was even increased in some mutant lines.

Conclusions:

RALDH1, RALDH2, and RALDH3 collectively play significant roles in ENS development and function.
RA metabolism by RALDH enzymes is critical for establishing normal ENS architecture and ensuring proper colon motility.
These findings underscore the importance of localized RA synthesis for complex developmental processes like ENS formation.