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Biomedical subjects

D L Price

Publications and source records attributed to D L Price.

At least 19 recordsLinked to original sources
PubMed1979

Hereditary spinal muscular atrophy in Brittany Spaniels: clinical manifestations.

A progressive neurologic disease was identified in a family of closely related Britanny Spaniel dogs. The disease developed in dogs less than 1 year old and characteristically resulted in paraspinal and proximal pelvic limb muscular atrophy. Neurologic examination, electrodiagnostic testing, and histologic studies indicated that the disease results from motor horn cell degeneration. A colony of affected dogs was established, and breeding studies incriminated an inherited basis for the disease.

Animals↗
PubMed1979

Chronic lead intoxication: effects on developing optic nerve.

The effects of chronic lead intoxication were studied by examining the optic nerve of mice given lead-containing mother's milk from day 1 to day 21 of life. Biochemical assays for myelin basic protein, 2',3'-cyclic nucleotide phosphodieterase, and cerebroside sulfotransferase showed that the total amount of myelin produced by the lead-exposed animals was decreased. Lead exposure did not alter the number of oligodendroglia or the relationship between axons and myelin sheaths. The hypomyelination was paralleled by a reduction in size of optic axons in the lead-exposed animals. The data suggest that chronic exposure to lead in developing mice results in a primary effect on neurons and that hypomyelination is secondary to reduction in axon size.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1979

Illumination of the dental operatory.

With the use of the two types of fixtures described in this paper and some precautions taken to reduce glare, the quality of lighting in the dental operatory can be improved.

Dental Offices↗
PubMed1978

Slow axonal transport of neurofilament proteins: impairment of beta,beta'-iminodipropionitrile administration.

beta,beta'-Iminodipropionitrile (IDPN) administration prevented normal slow axonal transport of [35S]methionine- or [3H]leucine-labeled proteins in rat sciatic motor axons. Ultrastructural and electrophoretic studies showed that the neurofilament triplet proteins in particular were retained within the initial 5 millimeters of the axons, resulting in neurofilament-filled axonal swellings. Fast anterograde and retrograde axonal transport were not affected. The IDPN thus selectively impaired slow axonal transport. The neurofibrillary pathology in this model is the result of the defective slow transport of neurofilaments.

Axonal Transport↗
PubMed1978

The development of intersegmental connections in embryonic spinal cord: an anatomic substrate for early embryonic motility.

This ultrastructural study of the embryonic chick spinal cord was designed to determine whether intersegmental inputs are formed before the closure of the reflex arc. Lesions were made in the thoracic cord of chick embryos at five days of incubation, when synapses are present in the ventral half of the cord, but before dorsal root afferents have made contacts in the central nervous system. Axons degenerating were observed in the upper brachial and lower lumbar regions of embryos sacrificed two days later. Synapses exhibiting degenerative changes were present up to six segments above and below the lesion. These observations were interpreted to indicate that: (1) intersegmental fibers connect the thoracic cord to brachial and lumbar areas by the fifth day of incubation; (2) early synapses contain both segmental and intersegmental connections; and (3) some intersegmental connections occur prior to the closure of the reflex arc. These morphologic studies, in conjunction with behavioral and electrophysiological data, strongly suggest that the early intersegmental connections are part of the propriospinal system. The development of these intersegmental tracts coincides with the onset of movement and thus provides an anatomical substrate for understanding embryonic motility.

Age Factors↗
PubMed1977

Regeneration of oligodendroglia during recovery from demyelinating disease.

Infection of mice with the JHM strain of mouse hepatitis virus causes demyelination as a result of a cytolytic infection of oligodendroglia. In recovery, animals show remyelination, which could result either from surviving oligodendrocytes extending their territory or by generation of new oligodendroglia. Electron microscopic autoradiographic studies with 3H-labeled thymidine demonstrate that the cells associated with remyelination are newly generated oligodendroglia.

Animals↗
PubMed1977

Myelinogenesis in optic nerve. A morphological, autoradiographic, and biochemical analysis.

Morphological, autoradiographic, and biochemical methods were used to study the time of appearance, distribution, and nature of sulfated constituents in the developing rat optic nerve. Electron microscope studies showed that myelination begins (6 days postnatal) shortly after the appearance of oligodendroglia (5 days postnatal). Over the ensuing 3 wk, myelination increased rapidly. During the 1st postnatal wk, mucopolysaccharides and glycoproteins were labeled with 35S and autoradiographs showed grains over arachnoidal cells, astroglia, and the glia limitans. These results indicated that astroglia synthesize sulfated mucopolysaccharides of the glia limitans. After the onset of myelination, however, the major portion of [35S]sulfate was incorporated into sulfatide. Autoradiographs showed a shift of radioactive grains from astroglia and arachnoidal cells to myelin, indicating that actively myelinating oligodendroglia incorporate [35S]sulfate into myelin sulfatide; there was a concomitant increase in the activity of cerebroside sulfotransferase. In addition, the increasing amounts of proteolipid protein and myelin basic protein corresponded with the morphological appearance of myelin. These results point to a strict correlation between the structural and biochemical changes occurring during myelination. This system provides a useful model for studies designed to evaluate the effects of various perturbations on the process of myelination.

Animals↗
PubMed1976

Electron microscopic autoradiographic studies of gliogenesis in rat optic nerve. I. Cell proliferation.

Electron microscopy and 3H-thymidine autoradiographic techniques were used to study the fine structure of proliferating cells in developing rat optic nerve. Before the closure of the optic canal almost all of the cells incorporating radioactive thymidine are ventricular cells, but after closure (16 days of gestation) the vast majority are differentiating astroblasts or oligodendroblasts. Labeled astroblasts show a range in their degree of differentiation; some cells lack 90 A cytoplasmic filaments while others have glial filaments and abundant cytoplasmic organelles. In contrast to astroblasts, all of the labeled oligodendroblasts are in the early stages of differentiation. The proliferation of oligodendroblasts starts at five days postnatal, approximately a day or two before the onset of myelination.During myelinogenesis a few of the labeled oligodendroblasts show presumptive connections to myelin sheaths. Microglial cells do not appear to play a major role in gliogenesis since they form less than 2% of all the labeled cells. The results of this study indicate that astroblasts and oligodendroblasts, rather than undifferentiated glioblasts, are the major source of macroglia. The finding that proliferating glia are in the processof differentiation agrees with recent studies which show that differentiated cells can divide.

Age Factors↗
PubMed1976

Electron microscopic autoradiographic studies of gliogenesis in rat optic nerve. II. Time of origin.

The time of origin for astrocytes and oligodendrocytes in rat optic nerve was studied by 3H-thymidine autoradiographic techniques similar to those used in dating the time of origin for neurons. This study shows that astrocytes are formed throughout late embryonic and all of postnatal development, while oligodendrocytes are generated only during the postnatal period. A few astroglia undergo their final cell division as early as 15.5 days of gestation, but most astrocytes are not generated until the first week of postnatal development. Although the final cell division for more than half of the astrocytes takes place before the end of the first postnatal week, fully mature, fibrous astrocytes are not observed in electron micrographs until after 14 days of age. This time lag implies that the differentiation of these early generated cells takes place gradually over a 2-to 3-week interval. Oligodendroglia begin their final division a day or two before the onset of myelination (6-7 days postnatal), but the vast majority are produced during the period of myelinogenesis. After almost all of the axons have been myelinated, oligodendrocytes are still being generated in small numbers. These late forming cells are generally less differentiated in appearance than those formed earlier; this suggests that the degree of differentiated of oligodendrocytes may be dependent upon the number of axons available for myelination. As with astrocytes, oligodendrocytes show a lag of about two weeks from the time of final cell division until they transform into morphologically differentiated cells. In transverse sections of the optic nerve heavily labeled neuroglia are randomly distributed, indicating there are no temporal-radial gradients for the individual cell types. This observation taken together with the other information obtained from the present and the previous study (Stoff et al., '76) strongly suggest that the factors controlling gliogenesis are different from those governing neuronogenesis.

Animals↗
PubMed1976

Botulinum toxin: mechanism of presynaptic blockade.

The mechanism of action of botulinum toxin was analyzed by the use of calcium ionophores and black widow spider venom. Addition of calcium ionophores to nerve-muscle preparations blocked by botulinum toxin did not increase the frequency of miniature end plate potentials. However, the spider venom elicited a barrage of miniature end plate potentials after blockade by botulinum. Electron micrographs of preparations treated with botulinum toxin and then the spider venom revealed clumping of synaptic vesicles at release sites in the otherwise depleted nerve terminals. These findings indicate that the action of botulinum toxin is not due to deficient storage of acetylcholine in vesicles or blockade of calcium entry into nerve terminals. They suggest that the toxin interferes with the acetylcholine release process itself, possibly by blocking exocytosis at the release sites.

Acetylcholine↗
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↗