Heterotopic neogenesis of skeletal muscle induced in the adult rat diaphragmatic peritoneum: ultrastructural and transplantation studies.

During the course of a mild chemical peritonitis, new skeletal muscle fibers develop and persist over a twelve-month interval in the diaphragmatic peritoneum. Light and electron microscopic studies revealed that the ectopic fibers developed from myoblasts and myotubes to fully differentiated muscle cells in the same manner as normally situated skeletal muscle. The ectopic fibers were separated from the intrinsic muscle by dense connective tissue and an elastic lamina.

Parenteral aluminum compounds produce a local toxic myopathy in rats: importance of the anion.

Aluminum lactate, injected in rats, produced skeletal muscle necrosis of diaphragm and abdominal wall subjacent to peritoneal surfaces. Deeper muscle cells (distal from inoculum) were less severely affected. Ultrastructural studies of diaphragm revealed inoculum coating collagen fibrils, aggregating next to muscle basal lamina and localized within phagocytes.

Ultrastructural features of the ventromedial region of the laminar nucleus in the red-eared turtle (Chrysemys scripta elegans).

The nuclei of the torus semicircularis, in particular the laminar nucleus, have been functionally implicated in sound localization, vocalization, and mating behavior. In the red-eared turtle the ventromedial region of the laminar nucleus (containing two discrete dense cellular areas and the surrounding neuropil) was examined electron microscopically in the present study. Neuronal cell bodies in the two cellular areas were different in size, shape, cytoplasmic constituents, and their relationship to each other.

An electrophysiologic and ultrastructural study of the phenylmethanesulfonyl fluoride protection against a delayed organophosphorus neuropathy.

The delayed organophosphorus neuropathy caused by diisopropylfluorophosphate (DFP) can be prevented by pretreatment with phenylmethanesulfonyl fluoride (PMSF). A single injection of DFP (2 mg/kg) into a cat femoral artery produced a delayed neuropathy in the injected leg. Clinical neurotoxic signs in the DFP treated leg were most prominent at 21 to 28 days after DFP administration: a high-step gait with some tip-toe walking.

A morphological study of the effect of glucocorticoid treatment on delayed organophosphorus neuropathy.

The delayed neuropathy caused by the organophosphate diisopropylfluorophosphate (DFP) can be minimized by a high dose glucocorticoid regimen started after exposure to DFP. In cats 21 days after an intraarterial injection (2 mg/kg) of DFP, morphologic alterations of neuromuscular junctions and myelinated intramuscular axons are evident. These alterations include the presence of extensive lamellar whorls in nerve axons and terminals, the disruption and retraction of nerve terminals from the synaptic cleft and a widening of secondary junctional folds with coincident dispersion of the basal lamina.

The effect of glucocorticoid treatment on denervated rat hemidiaphragm.

The degenerative process in phrenic nerve motor nerve terminals following nerve section was analyzed in rats that had previously been subjected to an intensive short term regimen of the steroid preparation triamcinolone. Morphological studies indicated that the onset time of degeneration was similar to that of untreated rats but less severe, and the time for maximal degenerative changes was increased. Concurrent to the preservation of motor nerve terminal structure under conditions of denervation, triamcinolone also induced myopathies in the diaphragm, the white muscle fibers being predominantly affected.

SEROTONIN: SYNTHESIS AND RELEASE FROM THE MYENTERIC PLEXUS OF THE MOUSE INTESTINE.

After injection of its radioactive precursor, 5-hydroxytryptophan, radioactive serotonin was biosynthesized and bound in the myenteric plexus of the mouse intestine. Addition of nonradioactive serotonin to preparations in vitro caused a net release of radioactive serotonin from the plexus. This release appeared to result from activity in the intramural nervous system of the intestine.