During development ex ovo, the avian mutant with an hereditary form of muscular dystrophy demonstrates biochemical, histochemical, and physiological (functional) abnormalities which may result from impaired muscle-nerve interaction. To investigate if impaired functional activity also characterizes the dystrophic process during development in ovo, limb motility, an index of embryonic functional muscle-nerve interaction, was compared between normal and dystrophic embryos from day 6E through day 16E. A highly significant reduction in this parameter was exhibited by dystrophic wings from day 11E to day 14E inclusive.
View Article and Find Full Text PDFIntraspecific chick/chick chimaeras were prepared by transplanting thoracic somitic mesoderm from donor chick embryos with hereditary muscular dystrophy to replace extirpated brachial somites of normal host embryos at stage 13 (48-52 h in ovo). Since the wings of unoperated dystrophic embryos exhibit significantly reduced motility between day-10 in ovo (day-10E) to day-15E, this parameter was used as a marker both to verify the viability of the transplant and to assess if the dystrophic phenotype of impaired functional activity is preserved in the mutant wing muscles innervated by brachial nerves of normal embryos. Our motility analyses of the chimaeras confirmed that transplanted thoracic somitic mesoderm gives rise to brachial musculature and that the experimental muscles maintained the inherent dystrophic phenotype.
View Article and Find Full Text PDFThe extent of interaction between brachial muscles and foreign (thoracic) nerves of the chick embryo was determined during an extended period of development in ovo from the perspectives of innervation pattern, function (motility analyses), muscle growth (quantitative analyses of muscle volume) and fibre-type expression (myosin-ATPase profiles). Results indicated that according to all parameters analysed, initially a compatible union existed between the foreign nerves and their muscle targets. During subsequent stages of development, deterioration of the once compatible relationship emerged, until eventually denervation of muscles, i.
View Article and Find Full Text PDFTreatment of gravid hamsters with 60/mg of retinoic acid on the 8th day of pregnancy resulted in facial skeleton defects in 100% of the survivors examined by alizarin staining at term. An investigation of the early stages in the development of these malformations indicated that the teratogen induced delayed and disorganized patterns of cranial neural crest cell migration as well as extensive death and damage of crest cells. The results demonstrate that retinoic acid provides a useful tool for studies in the pathogenesis of facial skeletal abnormalities in vivo.
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