Neuronal differentiation and myenteric plexus organization are delayed in gastroschisis: an immunohistochemical study in a rat model.

Gastroschisis is a malformation due to prenatal rupture of the abdominal wall and evisceration of the midgut. Intestinal loops are shortened, matted, and covered by a peel caused by the harmful effect of the amniotic fluid. Babies born with gastroschisis suffer from gastrointestinal dysmotility. The present aim was to verify whether the myenteric plexus is damaged in a rat model of gastroschisis. In the gastroschisis rat model fetus, the myenteric plexus was not yet organized in the well-defined ganglia and, in the most damaged loops, the neuronal cells were scattered or absent. Immunohistochemistry for alpha-internexin and peripherin (markers of neuronal maturity) gave results similar to those of earlier embryonic ages. These findings indicate a delay in neuronal differentiation and myenteric plexus organization that might play a role in the postnatal dysmotility observed in gastroschisis.