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  • 1995-1999  (2)
  • 1970-1974
  • 1,3-Di(2-tolyl)guanidine  (1)
  • ACTIVE OXYGEN METABOLISM  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 103 (1996), S. 661-669 
    ISSN: 1435-1463
    Keywords: σ1 Receptor ; (+)-N-allylnormetazocine ; 1,3-Di(2-tolyl)guanidine ; microdialysis ; acetylcholine ; hippocampus ; striatum ; regional differences ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We found that a receptor ligands differentially regulated the acetylcholine (ACh) neurotransmission in the rat brain. Acute administration of (+)-N-allylnormetazocine [(+)-SKF-10,047], a prototype σ1 receptor ligand, and 1,3-di(2-tolyl)guanidine (DTG), a non-specific σ receptor ligand, increased the extracellular ACh level in the rat hippocampus. This increase of hippocampal extracellular ACh level elicited by (+)-SKF-10,047 was more potent than that elicited by DTG. On the other hand, the striatal extracellular ACh level was slightly affected by (+)-SKF-10,047. In addition, DTG did not affect the striatal extracellular ACh level. Our previous studies have shown that both (+)-SKF-10,047 and DTG increased the extracellular ACh level in the rat frontal cortex. Taking all these data into consideration, the regulation of ACh neurotransmission by σ receptor ligands are different depending upon the brain region.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: COMPOUND 40/80 ; MAST CELL DEGRANULATOR ; GASTRIC MUCOSA ; MUCOSAL LESION RAT ; ACTIVE OXYGEN METABOLISM ; OXIDATIVE STRESS ; BLOOD FLOW ; ISCHEMIA-REPERFUSION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship between the changes of activeoxygen metabolism and blood flow and the formation,progression, and recovery of lesions was examined in thegastric mucosa of rats treated once with compound 48/80, a mast cell degranulator. Gastricmucosal lesions appeared 0.5 hr after compound 48/80treatment, became worst at 3 hr, and recovered fairlywell at 12 hr. Increases in gastric mucosal lipidperoxide content and xanthine oxidase andmyeloperoxidase activities and decreases in gastricmucosal vitamin E and hexosamine contents andSe-dependent glutathione peroxidase activity occurredwith the formation and progression of gastric mucosal lesions.These changes were attenuated with the recovery of thelesion. Gastric mucosal nonprotein SH content decreasedwith the formation of gastric mucosal lesions, and this decreased SH content returned to nearthe original level with lesion progression. No changesin gastric mucosal superoxide dismutase and catalaseactivities occurred with the formation, progression, and recovery of gastric mucosal lesions.Gastric mucosal blood flow decreased with the formationof gastric mucosal lesions, and this decreased bloodflow recovered with lesion progression. Serum serotonin concentration, an index of mast celldegranulation, increased with the formation of gastricmucosal lesions, and this increased serotonin level wasattenuated with lesion progression and recovery.Pretreatment with ketotifen, a connective tissue mast cellstabilizer, prevented the formation of gastric mucosallesions, the increases of gastric mucosal lipid peroxidecontent, xanthine oxidase and myeloperoxidase activities, and serum serotonin level; and thedecreases of gastric mucosal nonprotein SH content,glutathione peroxidase activity, and blood flow found at0.5 hr after compound 48/80 treatment. These results indicate that the changes of gastric mucosalactive oxygen metabolism and blood flow are closelyrelated to the formation, progression, and recovery ofgastric mucosal lesions in rats with a single compound 48/80 treatment. The present results alsosuggest that this compound 48/80-induced gastric mucosalinjury could be a kind of ischemia-reperfusion-inducedinjury occurring through degranulation of connective tissue mast cells.
    Type of Medium: Electronic Resource
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