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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 22 (1997), S. 735-741 
    ISSN: 1573-6903
    Keywords: Ascorbic acid ; chemiluminescence ; hydrogen peroxide ; microdialysis ; trauma ; uric acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Microdialysis probe insertion into rat cerebral cortex significantly affects the levels of redox-active substances in brain extracellular fluid. Ascorbic acid levels are high immediately after probe insertion, decline rapidly, and then rise as the rat recovers from anesthesia 5–8 hours after surgery. Uric acid is at a low level for 5 hours and then rapidly increases in parallel with ascorbic acid. High ascorbic acid levels immediately after probe insertion are likely due to a shift from intracellular to extracellular fluids, whereas the delayed increase in uric acid may be due to increased enzymatic formation. After removal from the brain, hydrogen peroxide (H2O2) in microdialysis samples produces catalase-sensitive oxidative chemiluminescence. Microdialysis samples also produce high level catalase-resistant chemiluminescence associated with ascorbic acid levels after penetration injury. Although ascorbic acid is likely an antioxidant at concentrations estimated to be in brain extracellular fluid, it may have prooxidant effects when complexed with transition metals released into the neuronal microenvironment during traumatic brain injury.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 17 (1992), S. 11-21 
    ISSN: 1573-6903
    Keywords: Local cerebral glucose use ; excitatory amino acids ; brain osmoregulation ; brain damage ; reactive oxygen species
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This overview presents data showing that glucose use increases and that excitatory amino acids (i.e., glutamate, aspartate), taurine and ascorbate increase in the extracellular fluid during seizures. During the cellular hyperactive state taurine appears to serve as an osmoregulator and ascorbate may serve as either an antioxidant or as a pro-oxidant. Finally, a unifying hypothesis is given for seizure-induced brain damage. This unifying hypothesis states that during seizures there is a release of excitatory amino acids which act on glutamatergic receptors, increasing neuronal activity and thereby increasing glucose use. This hyperactivity of cells causes an influx, of calcium (i.e. calcium stress) and water movements (i.e., osmotic stress) into the cells that culminate in brain damage mediated by reactive oxygen species.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 15 (1990), S. 541-545 
    ISSN: 1573-6903
    Keywords: Lithium ; inositol-1-phosphate ; inositol ; brain ; strain difference
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract LiCl-induced (5 mEq/kg) regional differences in the cerebral phosphoinositide (PI) cycle were studied by measuring inositol-1-phosphate (Ins-1-P), an, intermediate in the PI cycle, in male Sprague Dawley and Han/Wistar rats by gas chromatography/mass spectrometry. Control Ins-1-P levels were higher frontally than caudally in both rat strains. LiCl increased Ins-1-P levels 1.8 to 7.4 fold in different, regions of brain of Sprague Dawley rats but only 1.2 to 1.8 fold in Han/Wistar rats. This strain difference offers a way to compare the effects of lithium on PI metabolism versus receptor-G protein-phospholipase C coupling mechanisms.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 49 (1987), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Extracellular amino acid levels in the rat piriform cortex, an area highly susceptible to seizure-induced neuropathology, were determined by means of intracranial microdialysis. Seizures were induced by systemic administration of either soman (O-1,2,2-trimethylpropyl methylphosphonofluoridate), a potent inhibitor of acetylcholinesterase, or the excitotoxin kainic acid. Extracellular glutamate levels increased in animals with seizures shortly after administration of either convulsant, but this change was statistically significant only in the case of soman-treated animals. Extracellular taurine levels increased markedly, reaching two-and fourfold baseline levels during the second hour of soman-and kainic acid-induced seizures, respectively. Taurine levels did not increase in the subpopulation of soman-treated animals without seizures, a finding indicating that elevation of extracellular taurine level is seizure related. Thus, we propose that taurine efflux may be a physiological cellular response to neuronal changes produced by excito-toxic chemicals, either directly or as a consequence of seizures.
    Type of Medium: Electronic Resource
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