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Biomedical subjects

D L Price

Publications and source records attributed to D L Price.

29 records · Page 2Linked to original sources
PubMed1976

Experimental arthrogryposis caused by viral myopathy.

Immobilization of the embryo has been postulated to cause the joint deformities in arthrogryposis multiplex congenita (AMC). Experimental damage to the motor neurons or pharmacologic blockade of neuromuscular transmission has previously resulted in typical joint changes of AMC. In the present investigation, we have studied the effects of paralysis produced by a viral myopathy on joint development. Coxsackievirus A2 was injected intravenously into chick embryos on the seventh day of incubation. Within 48 hours, severe myositis and paralysis resulted. Electron microscopical and immunofluorescence techniques demonstrated virus in muscle cells. Within three to four days after infection, the muscle had virtually disappeared. Ankylosis of joints, corresponding to that seen in human AMC, occurred. This study shows that primary myopathy with paralysis can produce arthrogrypotic joint deformities. The possibility of a viral etiologic factor in some human cases of AMC should be considered.

Animals↗
PubMed1976

Fast axonal transport in motor nerve regeneration.

This report describes the fast transport of [3H]-leucine-labeled proteins in regenerating rat sciatic motor nerves. A normal rate of fast transport (383 +/- 33 mm/day) was present in the regenerating sprouts, as well as in the central stumps. The rapidly transported proteins passed the level of axotomy without impediment, and accumulated in the endings of the regenerating sprouts, as shown by electron microscope autoradiography. In addition, transported proteins accumulated in terminal neuromas. The relative amount of protein-incorporated radioactivity in the crest of transport in the regenerating nerves was increased compared to control nerves. These results are interpreted to suggest that the mechanism of fast transport is the same in regenerating nerves was increased compared to control nerves. These results are interpreted to suggest that the mechanism of fast transport is the same in regenerating sprouts as in normal axons; during regeneration fast transport appears to add newly synthesized materials to the growing tip.

Animals↗
PubMed1976

Glycine-specific synapses in rat spinal cord. Identification by electron microscope autoradiography.

Glycine, an inhibitory transmitter in spinal cord, is taken up into specific nerve terminals by means of a unique high-affinity uptake system. In this study, [3H]glycine was directly microinjected into rat ventral horn in vivo and electron microscope autoradiography used to localize the label in various anatomic compartments. Quantiative analysis showed that [3H]glycine labeled a high proportion of axosomatic and axodendritic synapses which presumably act to inhibit spinal motor neurons.

Animals↗
PubMed1975

Tetanus toxin: direct evidence for retrograde intraaxonal transport.

The neurotoxin tetanospasmin causes tetanus when it reaches the central nervous system. In this autoradiographic study, 125-I-labeled tetanospasmin was injected into the leg muscles of rodents, and the nerves supplying these muscles were crushed. The labeled toxin accumulated within axons on the distal side of the crush. This study provides direct evidence for retrograde axonal transport of a macromolecular toxin that acts at synapses in the central nervous system.

Animals↗
PubMed1975

Pathophysiology of chronic communicating hydrocephalus in dogs (Canis familiaris). Experimental studies.

A model designed to produce chronic communicating hydrocephalus in dogs has been developed in our laboratory. The animals tolerate the procedure well and the yield of animals with communicating hydrocephalus is high. Serial cisternograms show ventricular entry first with "clearing" and later with "stasis". CSF pressures are initially increased, but when the ventricles become enlarged the pressure falls into the normal range. Grossly there is generalized ventricular enlargement and, on histological studies, the ependyma is flattened and denuded. Periventricular edema occurs in the white matter. Autoradiographs show transependymal movement of protein. CSF production appears to be normal despite obstruction to flow of CSF to areas where resorption is greatest. Diversionary shunting probably produces relief of many of the neurological symptoms by providing an efficient pathway for the removal of CSF and thus by lessening edema and ventricular enlargement. A more appropriate treatment would appear to be a noninvasive method of decreasing CSF production. Only when the basic pathophysiological alterations of CSF production and absorption are understood will this be possible. We believe that this animal model affords us the opportunity of studying these mechanisms.

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PubMedDate not supplied

The pathogenesis of reactive axonal swellings: role of axonal transport.

The role of axonal transport in the pathogenesis of the axonal swellings which develop at the severed ends of transected axons was studied by electron microscopic (EM) autoradiography. Proteins carried by fast anterograde transport in rat sciatic nerves were labeled with [3H]-leucine or [3H]-fucose; [3H]-leucine, [3H]-fucose, and [125I]-tetanus toxin were used to label components of retrograde transport. After the labeling procedure, the nerves were ligated and 2 to 24 hours later the animals were perfused with fixatives. The axonal swellings in both the proximal and distal stumps contained densely packed membranous organelles. The transported radioactivity in the swellings was strictly associated with these organelles, particularly pleomorphic vesicles and branched tubules derived from smooth endoplasmic reticulum. The endogenous (tritiated) substances had a similar association with the organelle collections in both the proximal stump (fast anterograde transport) and in the distal stump (retrograde transport). The exogenous marker of retrograde transport (125I-tetanus toxin) had the same autoradiographic localization. These results suggest that fast anterograde and retrograde transport are very similar processes carrying predominantly membranous organelles and constituting a system of bidirectional fast transport. The accumulations of organelles in reactive swellings are interpreted as the consequence of the acute focal interruption of this system. Studies of axonal transport provide a means for investigation of the origin and fate of axonal organelles in pathologic processes.

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