Ncx (Enx, Hox11L.1) is required for neuronal cell death in enteric ganglia of mice

Taito Aoki, Ahmad Aulia Jusuf, Yoshinuri Iitsuka, Kaichi Isono, Takeshi Tokuhisa, Masahiko Hatano

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


Background/Purpose: Ncx (Enx, Hox11L.1)-deficient (Ncx-/-) mice develop mega-ileo-ceco-colon with a larger number of neuronal cells in the enteric ganglia. We investigated mechanisms related to this abnormality and directed our attention to the effects on gastrointestinal tract functions. Methods: The number of NADPH diaphorase or cuprolinic blue-positive neuronal cells in the enteric ganglia was examined during growth of the mice. Neuronal cell death of enteric ganglia was assayed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling. Function of the gastrointestinal tract was determined by measuring excretion time of the barium chloride given into the stomach. Results: The number of neuronal cells decreased in control mice older than 2 weeks, and neuronal cell death was evident in the ganglia. However, the number of neuronal cells did not decrease in Ncx-/- mice, and cell death was rare. Excretion time of barium chloride was prolonged in all Ncx-/- mice examined and was improved by the administration of an inhibitor of nitric oxide synthase. Conclusions: Ncx participates in cell death of enteric neurons. Motor abnormality of the gastrointestinal tract in Ncx-/- mice may be attributed to the large number of neuronal cells.

Original languageEnglish
Pages (from-to)1081-1088
Number of pages8
JournalJournal of Pediatric Surgery
Issue number6
Publication statusPublished - Jun 2007


  • Intestinal neuronal dysplasia
  • Ncx/Hox11L.1
  • Neuronal cell death


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