What do knockout models teach us about the enteric nervous system?
Eur J Pediatr Surg
; 13(3): 170-5, 2003 Jun.
Article
en En
| MEDLINE
| ID: mdl-12939701
ABSTRACT
Since the first histological studies, enormous strides have been made in understanding the genetics and cell biology of enteric nervous system (ENS) formation. Several mitogenic and trophic factors have been implicated in the process of neural cell proliferation and differentiation. A number of natural (piebald-lethal mice [s l], lethal spotting mice [ls], spotting lethal rats [sl]) or target (Gfralpha1-deficient mice, ret.k - mice, and NT-4 knockout mice) mutations have been reported to produce developmental defects in neural crest cell migration, differentiation or survival. Study of these mutations continues to provide new insights into this complex system. In the present investigation, we showed that a lack of basic fibroblast growth factor (FGF) or growth hormone (GH) leads to morphological abnormalities of the enteric nervous system. Because knockouts, neither of FGF nor of GH, produce enteric nervous system defects substantial enough to compromise the ability of the gut to support life, we postulate that FGF and GH affect only a relatively small subset of neurons and/or that compensatory effects of other growth factors might occur.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Enfermedades del Sistema Nervioso Autónomo
/
Ratones Noqueados
/
Sistema Nervioso Entérico
/
Modelos Animales de Enfermedad
/
Enfermedad de Hirschsprung
/
Enfermedades Intestinales
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Eur J Pediatr Surg
Asunto de la revista:
PEDIATRIA
Año:
2003
Tipo del documento:
Article
País de afiliación:
Alemania