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Biomedical subjects

T S Reese

Publications and source records attributed to T S Reese.

At least 127 records · Page 7Linked to original sources

Intercellular junctions in the reticular lamina of the organ of Corti.

Junctions between the cells in the reticular lamina of the organ of Corti were examined in thin sections and after freeze-fracturing to find a structural basis for the large ionic differences between the endolymph and perilymph. The apices of the cells in the reticular lamina are joined by a band of tight junctions spaced at 140 A intervals. Beneath this apical band the organization of the tight junctions depends on whether they join a supporting cell and a hair cell, or two supporting cells. At hair cell junctions with supporting cells, there is an extensive labyrinth of tight junctions enclosing lengthy, tortuous passages whose walls are composed of either multiple parallel or single junctions. At appositions between two supportinc cells, maculae or fasciae occludentes lie immediately beneath the apical bands of closely spaced tight junctions, near the top of the zonulae adherentia which are characteristic of appositions between supporting cells. The complexes of tight junctions, or zonulae occludentes, between extralaminar supporting cells differ from those in the reticular lamina. The extralaminar cells are joined by a band of four to seven branching, anastomotic tight junctions. Thus, these junctions are like zonulae occludentes in other tissues. The novel organizations of the tight junctions in the reticular lamina, different from those between the extralaminar supporting cells, suggests a special role for these junctions in the reticular lamina. Two sizes of gap junctions link, and presumably couple, supporting cells in the reticular lamina.

Animals↗

Similarity of junctions between plasma membranes and endoplasmic reticulum in muscle and neurons.

The structure of membranes at junctions between the plasma membrane and underlying cisterns of endoplasmic reticulum in amphioxus muscle and mouse cerebellar neurons was studied using the freeze-fracture technique. In amphioxus muscle, subsurface cisterns of sarcoplasmic reticulum form junctions with the surface membrane at the level of the sarcomere I bands. On the protoplasmic leaflet of the sarcolemma overlying these junctions were aggregates of large particles. On the protoplasmic leaflet of the membranes of cerebellar basket, stellate and Purkinie cells there were similar aggregates of large particles. In both tissues, the corresponding external membrane halves had arrays of pits apparently complementary to the aggregates of large particles. Cross fractures through junctions showed that the particle aggregates in neuronal and muscle membranes were consistently located over intracellular cisterns closely applied to the plasma membrane. Thus, a similar plasma membrane specialization is found at subsurface cisterns in mammalian neurons and amphioxus muscle. This similarity supports the hypothesis that subsurface cisterns in neurons, like those in muscle, couple some intracellular activity to the electrical activity of the plasma membrane.

Animals↗

Defective bud formation in human cells chronically infected with subacute sclerosing panencephalitis virus.

Human prostate cells chronically infected with the Mantooth strain of subacute sclerosing panencephalitis (SSPE) virus multiply normally, fuse only occasionally to form giant cells, and yet have twisted intracytoplasmic nucleocapsids. These cells are able to support replication of vesicular stomatitis virus, although they release only small amounts of SSPE virus. To determine why carrier cells do not produce virus, they were examined with techniques for surface replication, freeze-fracturing, and immunoperoxidase labeling with SSPE antibody. The surface of carrier cells, like that of productive cells, is characterized by ridges crowned with viral antigens and devoid of the intramembrane particles revealed by freeze-fracture techniques. Since surface ridges form where nucleocapsids attach to the membrane, the shape and length of ridges are indicative of the shape and length of the underlying nucleocapsid. Whereas ridges on productive cells are serpentine in shape, those on carrier cells are typically straight or hairpin shaped, and the hairpin ridges are twice as long as serpentine ridges on productive cells. Furthermore, the spacing between ridges on carrier cells is never as small as that in productive infections, so that continuous sheets of viral membrane are never formed. The majority of carrier cells lack the round viral buds observed in productive cells but have, instead, many elongated processes attached to the cell surface. Each of these processes contains one or two hairpin ridges overlying hairpin-shaped nucleocapsids. These "hairpin buds" are restricted to a single region of the carrier cell surface, whereas viral buds are distributed over the entire surface of productive cells. Thus, there are several structural defects in carrier cells that depend on the specific interaction of a certain viral strain with a certain cell type. These defects prevent the deployment of viral antigen in some regions of the cell surface, the formation of nucleocapsids of normal length, the coiling of attached nucleocapsids, and the consolidation of sheets of viral membrane into spherical buds with the nucleocapsids coiled inside. These defects may account for the failure of carrier cells to shed infectious virus.

Antigens, Viral↗

Junctions in the meninges and marginal glia.

The meninges of various mammals were prepared for examination with the electronmicroscope by thin sectioning or freeze-fracturing. Particular attention was given to the distribution of tight junctions in order to determine the basis for the meningeal barrier between the blood circulating in dural vessels and the cerebrospinal fluid in the subarachnoid space. While some dural blood vessels are fenestrated, those in the subarachnoid space are not and their component endothelial cells are joined by an extensive system of tight junctions. An extensive and continuous system of tight junctions was also found in a layer of specialized cells at the border of the arachnoid with the dura. This arachnoid barrier layer is apparently the only basis of the meningeal barrier because often cellular layers in the dura and arachnoid lack tight junctions although they are linked by gap junctions and desmosomes. In particular, tight junctions are lacking at the border of the "subdural space" which is actually a fascial plane within the dura. Tight junctions are also lacking between astrocytes at the surface of the brain but these cells are linked by gap junctions and a new type of intercellular junction. The distribution of these junctions, as well as assemblies of intramembranous particles at the astrocytic border, raises the question whether this layer might have a role in the exchange of certain substances between the brain and cerebrospinal fluid.

Animals↗

Structural changes in the membrane of vero cells infected with a paramyxovirus.

Vero cells productively infected with the Halle strain of measles virus have been studied by means of surface replication, freeze-fracturing, and surface labeling with horseradish peroxidase-measles antibody conjugate in order to examine changes in the structure of the cell membrane during viral maturation. Early in infection, the surfaces of infected cells are embossed by scattered groups of twisted strands, and diffuse patches of label for viral antigens cover regions marked by these strands. At later stages, when numerous nucleocapsids become aligned under the plasmalemmal strands, the strands increase in number and width and become more convoluted. At this stage, label for viral antigens on the surface of the cell membrane is organized into stripes lying on the crests of strands. Finally, regions of the membrane displaying twisted strands protrude to form ridges or bulges, and the freeze-fractured membrane surrounding these protrusions is characterized by an abundance of particles small than those found on the rest of the cell membrane. The fractured membranes of viral buds are continuous sheets of these small particles, and the spacing between both nucleocapsids and stripes of surface antigen in buds is less than in the surrounding cell membrane. Detached virus is covered with a continuous layer of viral antigen, has unusually large but no small particles on its membrane surfaces exposed by freeze-fracturing, and no longer has nucleocapsids aligned under its surface. Thus, surface antigens, membrane particles, and nucleocapsids attached to the cell membrane are mobile within the plane of the membrane during viral maturation. All three move simutaneously in preparation for viral budding.

Antigens, Viral↗

Serotonin storage in platelets: estimation of storage-packet size.

Storage-body diameter and volume, and the number of molecules of serotonin contained in a storage body, were estimated for blood platelets. In the human, 5.23 x 10(5) molecules of serotonin are contained in a storage body 198 nanometers in diameter, while in the cat, 31.2 x 10(5) molecules of this amine are contained in a storage body 298 nanometers in diameter.

Animals↗

Evidence for recycling of synaptic vesicle membrane during transmitter release at the frog neuromuscular junction.

When the nerves of isolated frog sartorius muscles were stimulated at 10 Hz, synaptic vesicles in the motor nerve terminals became transiently depleted. This depletion apparently resulted from a redistribution rather than disappearance of synaptic vesicle membrane, since the total amount of membrane comprising these nerve terminals remained constant during stimulation. At 1 min of stimulation, the 30% depletion in synaptic vesicle membrane was nearly balanced by an increase in plasma membrane, suggesting that vesicle membrane rapidly moved to the surface as it might if vesicles released their content of transmitter by exocytosis. After 15 min of stimulation, the 60% depletion of synaptic vesicle membrane was largely balanced by the appearance of numerous irregular membrane-walled cisternae inside the terminals, suggesting that vesicle membrane was retrieved from the surface as cisternae. When muscles were rested after 15 min of stimulation, cisternae disappeared and synaptic vesicles reappeared, suggesting that cisternae divided to form new synaptic vesicles so that the original vesicle membrane was now recycled into new synaptic vesicles. When muscles were soaked in horseradish peroxidase (HRP), this tracerfirst entered the cisternae which formed during stimulation and then entered a large proportion of the synaptic vesicles which reappeared during rest, strengthening the idea that synaptic vesicle membrane added to the surface was retrieved as cisternae which subsequently divided to form new vesicles. When muscles containing HRP in synaptic vesicles were washed to remove extracellular HRP and restimulated, HRP disappeared from vesicles without appearing in the new cisternae formed during the second stimulation, confirming that a one-way recycling of synaptic membrane, from the surface through cisternae to new vesicles, was occurring. Coated vesicles apparently represented the actual mechanism for retrieval of synaptic vesicle membrane from the plasma membrane, because during nerve stimulation they proliferated at regions of the nerve terminals covered by Schwann processes, took up peroxidase, and appeared in various stages of coalescence with cisternae. In contrast, synaptic vesicles did not appear to return directly from the surface to form cisternae, and cisternae themselves never appeared directly connected to the surface. Thus, during stimulation the intracellular compartments of this synapse change shape and take up extracellular protein in a manner which indicates that synaptic vesicle membrane added to the surface during exocytosis is retrieved by coated vesicles and recycled into new synaptic vesicles by way of intermediate cisternae.

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