[PGP 9.5 immunohistochemical study on the development of the enteric nervous system of trisomy 16 mouse embryos and their normal littermates].

OBJECTIVE

To study the development of the intestinal innervation of trisomy 16 mouse embryos and their normal littermates from embryonic days 13-18 (ED13-ED18).

METHODS

(1) Trisomy 16 mouse embryos used in this study were produced by crossing NMR-1 females with males carrying the two Robertsonian (Rb) translocation chromosomes Rb (11, 16) and Rb (16,17) 8 LubtwLub3. (2) Cytogenetic analysis: accurate ascertainment of trisomy 16 was provided by the demonstration of two Rb metecentric chromosomes and a count of 41 chromosome arms. (3) Rabbit-anti-human protein gene product 9.5 antibody was used in PAP and Avidin-biotin methods:

RESULTS

At ED13, neither nervous plexuses nor neurons were found in the gut of trisomy 16 mouse embryos and their normal littermates. And in the gut of normal littermates there appear only a scattering neurons with light staining nucleuses at ED14, the irregular network of the myenteric plexus composed of scattering distribution neurons and their processes at ED15 and the regular meshworks of the myenteric plexus with developed ganglia at ED16. However, in trisomy 16 mouse embryos at ED14-ED16, enteric nervous system (ENS) was composed of only some scattering neurons with different distribution density and size. The development of ENS was well in ED17-ED18 normal littermates. The developed myenteric plexus was composed of nervous meshworks with regular distribution. The submucosal plexus had irregularly shaped. The interconnecting strands were frequent visible between the myenteric and submucosal plexuses. In the gut of trisomy 16 mouse embryos the submucosal plexus was absent and the development and differentiation of the myenteric plexus were lower compared with their normal littermates. An important finding was that 5 mm aganglionic bowel was firstly found in the end of colon. In this study, the developed mesentery nervous fibers were persent and innervated in both type animal guts from ED14 to ED18.

CONCLUSIONS

It was original report to find the developmental delay of the ENS, absence of submucosal plexus and the aganglionic segment of colon ending in trisomy 16 mice, an animal model for Down syndrome.