[Observation on the development of stomach innervation in trisomy 16 mouse, an animal model for Down syndrome].

OBJECTIVE

To study the nervous development in the stomach of trisomy 16 mouse embryos and their normal littermates from embryonic days 13-18 (ED 13-ED 18) by using primary antibody against protein gene product (PGP) 9.5.

METHODS

(A) trisomy 16 mouse breeding; (B) trisomy 16 mouse embryos were confirmed by examining their chromosomes; (C) PGP 9.5 immunohistochemical method.

RESULTS

In normal littermates, the precursor cells from the neural crest migrated into stomach at ED13. Numerous nervous processes connected each other and formed early nervous networks at ED14. Original ganglia appeared in the muscular plexus with very simple arrangement at ED15. The developed myenteric and submucosal plexuses were found at ED16 and ED17 respectively. The myenteric plexus and the internal and external submucosal plexuses were differentiated at ED18. In comparison with the normal littermates, the trisomy 16 mice's stomach nervous development was much slower. Their immature neurons did not appear in the stomach until ED14; the development and differentiation of stomach nervous plexuses were delayed. A clear link was noted between the development of stomach plexuses and the density of PGP 9.5 immunostaining. A semiquantitative analysis and rank sum test of the data showed that the trisomy 16 mouse embryos were markedly retarded in nervous development of stomach, compared with their normal littermates (P<0.05).

CONCLUSION

Trisomy 16 mouse, as an animal model for Down syndrome, has abnormality not only in several systems and organs but also in stomach innervation. This is the first report on delayed nervous development in the stomach of trisomy 16 mice.