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Biomedical Research

Brief: Are animals a suitable model for motility disorders? Current views upon ENS development and own experiences with a FGF-knock-out model

Author(s): C.I. Hagl, E. Wink, K. Kr�nzle, A. H�nsgen, M. Diener, N. Gretz, K.-H. Schäfer

Vol. 14, No. 1 (2003-01 - 2003-06)

C.I. Hagl, E. Wink, K. Kr�nzle, A. H�nsgen, M. Diener, N. Gretz, K.-H. Schäfer

Correspondence to:

Professor K.-H. Schäfer
Department of Pediatric Surgery
Rupprechts-Karls-Universität Heidelberg
Clinical Faculty Mannheim
Germany

Since the first histological studies, performed by Lane in 1966 enormous strides have been made in understanding the genetics and cell biology of ENS formation. For Hirschsprung´s disease (HSCR) and intestinal neuronal dysplasia type B (INDB) in humans, several rodent models like lethal spotted (ls/ls) mice, piebald-lethal mutant mice (lsl/lsl), lethal spotted (ls/ls) rats or Ret, Gdnf and Gfra1 knock-out mice, are known. Many of these genetic abnormalities or knock-out animals give a phenotype similar or identical to HSCR.

Several mitogenic and trophic factors have been implicated in the process of neural cell proliferation and differentiation. These include especially the GDNF family and other potent neurotrophins such as NT3 and fibroblast growth factor (FGF) for which so far stimulation of neurogenesis and survival of enteric neurons has been demonstrated in vitro. In this review several mutants and knock-out models were described and first data of FGF influence in vivo based on a FGF-knock-out model were presented.

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