Biomedical subjects

J Rosenbluth

Publications and source records attributed to J Rosenbluth.

77 records · Page 5Linked to original sources

PubMed1966

Redundant myelin sheaths and other ultrastructural features of the toad cerebellum.

Some of the myelin sheaths in the cerebellum of normal adult toads exhibit extensive evaginations of their full thickness. These redundant flaps of myelin are collapsed; i.e., they contain no axon and have no lumen. They extend away from the parent axonal myelin sheaths and tend to enfold other myelinated fibers or granule cell perikarya, producing bizarre configurations of myelin and what appear to be partially or completely myelinated cell bodies. In some instances, only the redundant flap of myelin appears in the plane of section, and its attachment to an axonal myelin sheath in another plane is only inferred. Single lamellae of myelin also tend to invest cerebellar granule cells and other processes, and these too appear to fold on themselves producing two- or four-layered segments. It is suggested that there are two phases of myelinogenesis: an initial "wrapping" phase, followed by a prolonged second phase during which internodes of myelin increase in both length and girth by a process other than wrapping, and that the occurrence of redundant myelin sheaths may reflect overgrowth of myelin during the second phase. Observations on the general organization of the toad cerebellum and on the ultrastructural cytology of its layers are also presented.

Animals↗

PubMed1965

Ultrastructural organization of obliquely striated muscle fibers in Ascaris lumbricoides.

The somatic musculature of the nematode, Ascaris, is currently thought to consist of smooth muscle fibers, which contain intracellular supporting fibrils arranged in a regular pattern. Electron microscopic examination shows that the muscle fibers are, in fact, comparable to the striated muscles of vertebrates in that they contain interdigitating arrays of thick and thin myofilaments which form H, A, and I bands. In the A bands each thick filament is surrounded by about 10 to 12 thin filaments. The earlier confusion about the classification of this muscle probably arose from the fact that in one longitudinal plane the myofilaments are markedly staggered and, as a result, the striations in that plane of section are not transverse but oblique, forming an angle of only about 6 degrees with the filament axis. The apparent direction of the striations changes with the plane of the section and may vary all the way from radial to longitudinal. A three-dimensional model is proposed which accounts for the appearance of this muscle in various planes. Z lines as such are absent but are replaced by smaller, less orderly, counterpart "Z bundles" to which thin filaments attach. These bundles are closely associated with fibrillar dense bodies and with deep infoldings of the plasma membrane. The invaginations of the plasma membrane together with intracellular, flattened, membranous cisternae form dyads and triads. It is suggested that these complexes, which also occur at the cell surface, may constitute strategically located, low-impedance patches through which local currents are channeled selectively.

Animals↗

PubMed1965

Ultrastructure of somatic muscle cells in Ascaris lumbricoides. II. Intermuscular junctions, neuromuscular junctions, and glycogen stores.

Somatic muscle cells of Ascaris lumbricoides consist of three differently specialized components referred to as the fiber, which contains the contractile apparatus (described previously), the belly, and the arm. The belly is shown to be a sac of glycogen, which is depleted during starvation of the animal. The arm extends to a nerve cord where it establishes a myoneural junction characterized by giant mitochondria and clusters of vesicles in the nerve fibers and by a 500 A neuromuscular gap. The arms, which have been shown to be "electrically interconnected" in the vicinity of the nerve cord, form "tight junctions" with one another in just this region. At high magnification, these junctions can be resolved into several types. In some there is fusion of the outer leaflets of the membranes with formation of an intermediate line. Others resemble septate desmosomes in that a residual extracellular space approximately 20 A in width remains between the membranes, but the outer leaflets are interconnected across the gap. It is suggested that the term "tight junction" encompasses a variety of structures distinguishable only at high magnification and that the different variations are not necessarily equivalent functionally.

Ascaris↗

PubMedDate not supplied

Antibody-mediated CNS demyelination: focal spinal cord lesions induced by implantation of an IgM anti-galactocerebroside-secreting hybridoma.

O1 hybridoma cells, which secrete an IgM antigalactocerebroside, were implanted into the spinal cord of cyclosporine-treated juvenile or adult rats, and the animals were sacrificed approximately 2-3 wk later. About half the recipient animals developed myelin lesions. In some, sharply circumscribed foci of demyelination formed within the dorsal columns. Cellular reaction consisted of macrophages containing refractile globules in the parenchyma and within enlarged perivascular spaces as well as thickened endothelial cells. "Shadow plaques" also developed, i.e. regions in which axons were surrounded by thin myelin sheaths, compatible with remyelination. In addition, we found damaged axons, some of which were swollen with organelles, comparable to the enlarged axon profiles seen at sites of constriction or interruption. Compromise of the blood-brain barrier at sites of hybridoma growth was demonstrated by extravasation of Evans blue dye. Discontinuation of cyclosporine was followed by an anti-hybridoma, complement-fixing antibody response within 2-3 d. This model of focal CNS demyelination and remyelination, with evidence of some axon damage, is mediated by a defined IgM antiglycolipid monoclonal antibody secreted within the spinal cord parenchyma. The lesions, which are similar to those of multiple sclerosis, probably result from the interaction between the intrathecally secreted IgM antibody and complement entering from the circulation at foci of compromised blood-brain barrier plus activation of endogenous or hematogenous macrophages via their complement receptors.

Age Factors↗

PubMedDate not supplied

A brief history of myelinated nerve fibers: one hundred and fifty years of controversy.

The early controversies over myelinated nerve fibers focused on whether nerves are hollow or not, whether the fatty "marrow" (myelin) is inside the nerve fiber or around it, whether myelin is secreted by the axon or formed by another cell, whether nerve fibers are discrete or part of a syncytial network, whether nodes of Ranvier are present in central myelin or only in peripheral myelin. Since Geren's seminal discovery that peripheral myelin is formed by the Schwann cell plasma membrane wrapped around the axon, the focus has shifted. Myelin is clearly a living cell appendage, and the myelin sheath is dependent upon intercellular interactions not only during its formation, but throughout its lifetime and during pathological processes affecting either the axon or the myelin-forming cell. The myelinated fiber is a functional unit, an exquisite symbiosis, whose ability to perform optimally, in some cases whose very survival, depends on the effects the respective cells exert on one another. How are these interactions mediated? Which structures and functions depend on such interaction and which are independent of it? How do cells of the size and shape of myelin-forming cells cope with their metabolic demands and support their most distal components? What are the mechanisms and mutual consequences of demyelination or axonopathy? Relevant studies have burgeoned with the development of molecular biological and genetic engineering methods, and with improvements in microscopy, in vitro culture and specific immunostaining methods. This introductory essay provides an overview of the structural background and continuing controversies relevant to the articles that follow, which represent a sampling of current work and present new information on the molecular structure, function and pathology of myelin and axoglial interactions.

Animals↗