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PubMed1984

Disease expression in +-/+- ----mdg/mdg mouse chimeras: evidence for an extramuscular component in the pathogenesis of both dysgenic abnormal diaphragm innervation and skeletal muscle 16 S acetylcholinesterase deficiency.

Homozygous mdg/mdg mice die at birth and express a syndrome of abnormalities, the most striking of which is a gross failure of skeletal muscle development. Recently, additional abnormalities in the development of nerve-muscle relationships have been recognized; in particular, on muscle fibers within the diaphragm, motor end plates are inappropriately dispersed and, in all muscles, there is a paucity of the 16 S form of acetylcholinesterase (AChE). These abnormalities could result entirely as secondary consequences of the primary muscle defect or from expression of the mdg defect in additional cell types, e.g., motor neurons. To determine if the muscle genotype alone is responsible for these defects in dysgenic mice, chimeras composed of both dysgenic and normal cells have been investigated. Different glucosephosphate isomerase variants existed in the mdg/mdg and normal cells comprising these chimeras and the mutant, normal, or mosaic genotypes of chimera diaphragm and skeletal muscle was estimated by measuring the relative proportions of each isozyme. In two chimeras, the diaphragm innervation pattern was revealed by AChE cytochemistry and in both, discrete regions of abnormally dispersed and normally restricted motor end-plate zones were observed. No correlation between these patterns of innervation and the assessed genotype of the muscle fibers existing in each area was observed. The relative 16 S AChE content in the limbs of four chimeras was found to range from 2.5 to 42.0%. Here also, no correlation between 16 S AChE content and the muscle genotype was observed. The results of these investigations are not consistent with a model of mdg/mdg pathogenesis in which only the skeletal muscle is primarily affected; an extramuscular deficiency responsible for at least part of the full mdg/mdg syndrome is therefore suggested.

Acetylcholinesterase↗
PubMed1988

Changes in myosin and C-protein isoforms proceed independently of the conversion to singly innervated neuromuscular junctions in developing pectoral muscle.

Changes in contractile protein expression during myogenesis are usually categorized as developmentally programmed or neuronally dependent. Studies on aneurogenic chick embryos indicated that the neuronally dependent phase begins at about Embryonic Day 15, immediately prior to the fetal transition in myosin and C-protein expression. The prime candidate for the neuronal event that induces the fetal transition is the conversion to the adult form of singly innervated neuromuscular junctions (NMJs), which occurs contemporaneously with the fetal transition. Using curare to inhibit the conversion to focal innervation, we find that the fetal transition proceeds unimpaired, demonstrating that there is no causal link between the fetal transition and the conversion to focal innervation. Furthermore, because the doses of curare used inhibit motor activity by more than 80%, the fetal transition can occur in the absence of normal levels of motor activity. These observations show that the fetal transition in ovo is not induced by either a specific change in innervation or use. Rather, the dependence on innervation seems to be a consequence of the need for muscle activity to prevent atrophy, and the fetal transition appears to have characteristics more like the preprogrammed contractile protein transitions that precede it.

Acetylcholinesterase↗