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Dilations of the sarcotubular system and misaligned myofilaments have been reported as early indicators of muscular dystrophy in skeletal muscle. Since the developing tubular component is believed instrumental in initial myofilament alignment during myogenesis, tubular development is evaluated using normal and dystrophic chick embryo skeletal muscle and cultures of normal and dystrophic embryonic pectoral muscle incubated in the presence of horse spleen ferritin. Comparisons of the findings show that periodic tubules are absent from dystrophic somitic muscle and that invaginating tubules from the sarcolemma are found in fewer, randomly located areas of dystrophic pectoral muscle cells. The results indicate that the tubular component is not involved in the bizarre vesiculations seen in mature dystrophic muscle, however, the malalignment of dystrophic myofilaments is probably the result of the poorer development of the T system in this muscle.

Pectoral muscle from normal and dystrophic New Hampshire chicken embryos was dissociated and grown in vitro. Marked differences between the two types of cell cultures were observed with the light and electron microscopes during early myogenic stages. The diseased myoblasts assumed a polarized affect and fused into smaller and fewer myotubes. Pseudostraps rather than true muscle straps were often seen in diseased cultures. There was also a delay in the appearance of myosin containing thick myofilaments in differentiating dystrophic muscle cells.

New Hampshire chickens, homozygous for inherited muscular dystrophy, display clinical manifestations at an early age. A fine structural examination of embryos from this strain shows marked degenerative changes four days prior to hatching. The Z bands appear to dissolve progressively to the point where finally the myofibrils become uniformly dense with no detectable banding patterns.

In New Hampshire chickens, the primary clinical symptom of dystrophy is limitation of wing motility. Examination of the brachial-level motor unit in chick embryos homozygous for dystrophy reveals abnormalities in both muscular and neural components. Wing motility in these embryos is abnormal as early as six days, and there is a corresponding lack of differentiation of the pectoralis major muscle. The findings suggest that delayed development of brachial-level neuronal pathways is responsible for the decreased wing motility and early degeneration of the pectoral muscle.

By use of horseradish peroxidase (Sigma Type II) as a vascular tracer the competence of the bursal microvasculature was evaluated in 15-day-old chicks. Within 5 min circulation time tracer could be identified only within the vascular tree with no leakage into the perivascular or extracellular spaces. After 10 min circulation time tracer was no longer present in the bursal vessels. Since no tracer was ever identified among the parenchymal elements of the organ these data suggest that a blood-organ (blood-bursa) barrier may exist similar to that found in thymus and brain.

The mechanism of plasma membrane turnover was investigated using the duckling salt gland as a model system. Feeding fresh water to salt-stressed ducklings results in a decrease in the Na, K-ATPase in salt gland to non-stressed levels in about 7 days, as measured by ATP hydrolysis and 3H-ouabain binding. Electron micrographs reveal that this is accompanied by a decrease in plasma membrane infoldings on the basal and lateral borders of gland secretory cells. Simultaneously there is an increase in filamentous material and a rise in acid phosphatase and peptidase activities in these cells. Cytochemistry shows that the acid phosphatase activity is mostly associated with the basal or basolateral regions of secretory cells. These ovservations could indicate that the removal of plasma membrane components is accomplished by internalization and digestion within the secretory cells.

The nine-banded armadillo possesses a salivary bladder which is a dilated portion of the main duct of the submandibular gland at its origin. The wall of the bladder is composed of an epithelium, a submucosa and a thick coat of skeletal muscle. The ultrastructure of the epithelium reveals that it is complex and consists of three cell types: 1) principal cells, 2) light cells, and 3) basal cells. The general organization of the epithelium suggests that it is a transporting type of epithelium such as that found in the amphibian and reptilian and reptilian urinary bladders and the mammalian gall bladder. The submucosa is composed primarily of densely-packed collagen fibers. The skeletal muscle is very vascular and richly innervated.