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Biomedical subjects

T Maeda

Publications and source records attributed to T Maeda.

At least 1,351 records · Page 75Linked to original sources
PubMed1982

Sites of actions of adenosine in intrinsic cholinergic nerves of ileal longitudinal muscle from guinea pig.

The sites of presynaptic actions of adenosine on electrically stimulated longitudinal muscle strip of guinea pig ileum were studied with a special dual organ bath. Local stimulation (0.1 Hz) of the anal part of the strip induced a twitch response in the stimulated part and in the non-stimulated oral part; both of these twitch responses were depressed by an application of adenosine to the anal, stimulated part of the strip. The present results suggested that electrical stimulation applied to the anal part of the strip travelled along the network of Auerbach's plexus in the oral direction, and adenosine might depress such conduction in cholinergic nerve fibers in addition to nerve terminals.

Adenosine↗
PubMed1982

Immunocytochemical study on cholera toxin binding sites by monoclonal anti-cholera toxin antibody in neuronal tissue culture.

An indirect method of immunocytochemistry showed that cholera toxin and its B-subunit served as specific neuronal surface markers in conjunction with monoclonal anti-cholera toxin and FITC labeled anti-mouse Fab. The cell types which get specifically stained in culture were peripheral neurons from dorsal root ganglion cells, superior cervical ganglion cells, and cerebral neurons, all of which were rat tissue, and NGF-treated PC12 cells. Non-neuronal cells, i.e. Schwann cells, fibroblasts and glia cells, were not stained. This method can, therefore, be used to distinguish neurons from non-neuronal cells in neuronal tissue cultures, as in the case of tetanus toxin described in the literature.

Animals↗
PubMed1982

Noradrenergic axon terminals in the substantia gelatinosa of the rat spinal cord: an electron-microscopic study using glyoxylic acid-potassium permanganate fixation.

The noradrenergic terminals in the substantia gelatinosa of the dorsal horn of the cervical spinal cord of the rat were investigated by means of the histofluorescence technique and electron-microscopic cytochemistry using the glyoxylic acid-KMnO4 fixation technique. In accordance with the topographical distribution of fluorescent catecholaminergic fibers, noradrenergic terminals containing small granular vesicles were frequently observed electron microscopically in the outer layer of the substantial gelatinosa. These terminals were most frequently found to appose (without showing typical synaptic features, small-caliber dendrites, spine apparatus, and rarely, large caliber dendrites. Only in a few cases, the noradrenergic terminals exhibited typical synaptic contacts with dendritic elements of small size. In addition, noradrenergic terminals apposed non-noradrenergic terminals containing small agranular vesicles. In rats bearing surgical lesions of the dorsal roots, no noradrenergic terminal were found in contact with the degenerated axon terminals in the substantia gelatinosa. These findings suggest that the noradrenergic afferents to the substantia gelatinosa may exert their influence on sensory transmission via dorsal horn cells.

Animals↗
PubMed1982

The regeneration of cholinesterase-positive structures in the process of burn wound healing in the skin of the guinea-pig.

The regeneration of acetylcholinesterase-positive structures was studied during the process of third-degree burn wound healing in the skin of guinea-pigs. The procedure in this study generally followed the histochemical thiocholine technique of Karnovsky and Roots (1964) with slight modification. Acetylcholinesterase activity in the skin was found to disappear from the burn wound including its margin within 14 days post burn. True regeneration of acetylcholinesterase activity became visible after 21 days post burn. The cholinergic fibres reinnervating arterioles became visible on the twenty-first day, and thereafter gradually increased in number and staining intensity at the deep region of scar margins. The cholinergic fibres detected at the upper region of the scar centre on the twenty-first day disappeared on the twenty-eighth day. Such denervation of the cholinergic fibres may be elicited by the absence of the target organs or by a dense collagenous scar which induces degenerative changes in regenerated nerves. The denervation of cholinergic nerve fibres occurred in association with degeneration of the target organs. On the other hand, the regeneration of the cholinergic nerve fibres was not always associated with the regeneration of the target organs, but occurred later than that of the target organs.

Acetylcholinesterase↗
PubMed1982

The regeneration of the sympathetic catecholaminergic nerve fibers in the process of burn wound healing in guinea pigs.

In the present study, morphological alterations of cutaneous catecholaminergic nerve fibers in the process of burn wound healing have been investigated by using glyoxylic acid induced fluorescence histochemistry. The sympathetic denervation is detected within 48 hr after burns as well as in various excisions. The regenerating sympathetic fibers are observed on the 7th day after burns. These regenerating fluorescent fibers seem to develop in accordance with the regeneration of blood vessels in the wound margins at various stages of healing. Regenerating sympathetic fibers gradually increase in number and the maximum density of these fibers is found approximately at 2 weeks after burns. Thereafter, the density of the fibers gradually decreases to less than that of sympathetic innervation of intact skin. On the 14th day after burns, dense regenerating fibers are observed around the regenerated arterial vessels in the deep granulation tissue of the wound margins. These fibers may correlate with the degeneration of regenerated blood vessels in the center of the wound because of contracting the blood vessel of the wound margins. Moreover, dense collateral sprouting of regenerating fibers is observed around the degenerative blood vessel in the center of the wound on the 16 day after burns. This sprouting occurs not because of searching after a new target organ following the degeneration of the target organ but because of playing important roles in certain functions during wound healing.

Animals↗
PubMed1982

Infectious cell entry mechanism of influenza virus.

Interaction between influenza virus WSN strain and MDCK cells was studied by using spin-labeled phospholipids and electron microscopy. Envelope fusion was negligibly small at neutral pH but greatly activated in acidic media in a narrow pH range around 5.0. The half-time was less than 1 min at 37 degrees C at pH 5.0. Virus binding was almost independent of the pH. Endocytosis occurred with a half-time of about 7 min at 37 degrees C at neutral pH, and about 50% of the initially bound virus was internalized after 1 h. Electron micrographs showed binding of virus particles in coated pits in the microvillous surface of plasma membrane and endocytosis into coated vesicles. Chloroquine inhibited virus replication. The inhibition occurred when the drug was added not later than 10 min after inoculation. Chloroquine caused an increase in the lysosomal pH 4.9 to 6.1. The drug did not affect virus binding, endocytosis, or envelope fusion at pH 5.0. Electron micrographs showed many virus particles remaining trapped inside vacuoles even after 30 min at 37 degrees C in the presence of drug, in contrast to only a few particles after 10 min in vacuoles and secondary lysosomes in its absence. Virus replication in an artificial condition, i.e., brief exposure of the inoculum to acidic medium followed by incubation in neutral pH in the presence of chloroquine, was also observed. These results are discussed to provide a strong support for the infection mechanism of influenza virus proposed previously: virus uptake by endocytosis, fusion of the endocytosed vesicles with lysosome, and fusion of the virus envelope with the surrounding vesicle membrane in the secondary lysosome because of the low pH. This allows the viral genome to enter the target cell cytoplasm.

Animals↗