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Updated: May 30, 2026

Immunostaining to Visualize Murine Enteric Nervous System Development
Published on: April 29, 2015
Morphological alterations of the enteric nervous system in young male patients with rectal prolapse
Dimitri Zorenkov1, Susanne Otto, Martina Böttner
1Department of Anatomy, Christian Albrechts University in Kiel, Otto-Hahn-Platz 8, 24118, Kiel, Germany.
Objectives:
The pathogenesis of rectal prolapse (RP) defined by a circumferential, full-thickness invagination of the rectal wall into the anal canal is controversial. RP is normally encountered in elderly women and attributed to several etiological factors (e.g., advanced age, pudendal nerve injury, laxity of supporting ligaments). RP affecting young male patients is unlikely to be explained by these factors and may be due to a rectal motility disorder. Therefore, the enteric nervous system (ENS) as key regulator of intestinal motility was evaluated by a systematic morphometric analysis.
Patients And Methods:
Full-thickness rectosigmoid specimens obtained from young male patients with symptomatic RP (n = 5) and male controls (n = 15) were processed for conventional histology and immunohistochemistry using anti-HuC/D as pan-neuronal marker. Enteric ganglia, nerve and glial cells were quantified separately in the myenteric (MP) and submucosal plexus (SMP).
Results:
Compared to controls, patients with RP showed significantly (p < 0.05) increased mean ganglionic area both in MP and SMP, increased mean neuronal content of submucosal ganglia, and nearly threefold higher frequency of submucosal ganglia containing ≥7 neurons.
Conclusion:
The morphometric analysis reveals distinct quantitative alterations of the ENS in young male patients with RP mainly characterized by submucosal hyperganglionosis similar to histopathological features described in intestinal neuronal dysplasia. The data give evidence that RP in this unusual subgroup is associated with morphological changes of enteric ganglia which may contribute to the development of RP and complement established etiological concepts.
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