Myenteric plexus alterations downstream from a prenatal intestinal obstruction in a rat model

Neurosci Lett. 2009 Sep 18;461(2):126-30. doi: 10.1016/j.neulet.2009.06.009. Epub 2009 Jun 17.

Abstract

The enteric nervous system maturation occurs during embryonic life and continues after birth. Some prenatal events on the digestive tract such as intestinal atresia have been shown to dramatically alter this maturation. Thus, we developed a fetal rat model of intestinal atresia by surgically obstructing the small bowel at embryonic day E18. Fetuses were removed at day E21, and small bowels sections were examined by immuno-histochemistry. Synaptophysin and smooth muscle actin staining was used to define the cellular aspect. Labeling revealed marked alterations of the myenteric plexus in the lower extremity of the occluded small bowel. At day E21, the myenteric plexus of the lower part and the 2 muscle layers surrounding it, retained the staining pattern observed at day E17. This cellular pattern was classified as: immature (aspect at day E17) vs. mature (aspect of day E21) by 3 pathologists not familiar with the study. The number of samples with an immature cellular pattern at the lower end of the occluded bowel was different from that observed for the upper end (Mac Nemar test, p<0.008). Our study suggests that a prenatal obstruction induces a maturation delay of the myenteric plexus downstream of the obstruction. This might be important for pediatric purposes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Female
  • Fetal Diseases / pathology
  • Immunohistochemistry
  • Intestinal Atresia / complications
  • Intestinal Atresia / embryology*
  • Intestinal Obstruction / complications
  • Intestinal Obstruction / embryology*
  • Intestine, Small / embryology
  • Intestine, Small / innervation*
  • Muscle, Smooth / embryology
  • Muscle, Smooth / innervation
  • Myenteric Plexus / abnormalities*
  • Myenteric Plexus / embryology
  • Pregnancy
  • Pregnancy Complications / pathology*
  • Rats
  • Synaptophysin / metabolism

Substances

  • Actins
  • Synaptophysin