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  • Taurine release  (2)
  • Cerebral protein synthesis  (1)
  • Chloride flux  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 14 (1971), S. 48-60 
    ISSN: 1432-1106
    Keywords: Hyperphenylalanaemia ; Tyrosine ; Blood-brain exchange ; Cerebral protein synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An account is given of an experimental design and a computing procedure for in vivo measurement of the blood-tissue exchange of amino acids and the metabolic rate of tissue proteins with radioactively labelled amino acids. The method was used for evaluation of the exchange rates of tyrosine between the plasma and the brain and between the free and protein-bound tyrosine compartments in the brain of adult rats in experimental hyperphenylalanaemia and hypertyrosinaemia. Hyperphenylalanaemia inhibited the exchange of tyrosine between plasma and brain. In both hyperphenylalanaemic and hypertyrosinaemic rats the rate of synthesis of the cerebral proteins fell. Alterations in the intracerebral pool of free amino acids produced by excessive loading with phenylalanine or tyrosine are suggested as the cause of the impairment of cerebral protein synthesis.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Amino acids 17 (1999), S. 323-334 
    ISSN: 1438-2199
    Keywords: Amino acids ; Taurine release ; Cerebellar granule cells ; Celldamaging conditions ; Glutamate receptors ; Veratridine ; Potassium stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of taurine from cultured cerebellar granule neurons was studied in different cell-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress and in the presence of free radicals. The effects of both ionotropic and metabotropic glutamate receptor agonists on the release were likewise investigated. The release of [3H]taurine from the glutamatergic granule cells was increased by K+ (50mM) and veratridine (0.1 mM), the effect of veratridine being the greater. Hypoxia and ischemia produced an initial increase in release compared to normoxia but resulted in a diminished response to K. Hypoglycemia, oxidative stress and free radicals enhanced taurine release, and subsequent K− treatment exhibited a correspondingly greater stimulation. A common feature of taurine release in all the bove conditions was a slow response to the stimulus evoked by K+ and particularly to that evoked by veratridine. All ionotropic glutamate receptor agonists potentiated taurine release, but only the action of kainate seemed to be receptor-mediated. Metabotropic receptor agonists of group I slightly stimulated the release. The prolonged taurine release seen in both normoxia and cell-damaging conditions may be of importance in maintaining homeostasis in the cerebellum and reducing excitability for a longer period than other neuroprotective mechanisms.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1438-2199
    Keywords: Amino acids ; Taurine release ; Metabotropic glutamate receptors ; Hippocampal slices ; Adult ; Developing mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The inhibitory amino acid taurine has been held to function as an osmoregulator and modulator of neural activity, being particularly important in the immature brain. lonotropic glutamate receptor agonists are known markedly to potentiate taurine release. The effects of different metabotropic glutamate receptor (mGluR) agonists and antagonists on the basal and K+-stimulated release of [3H]taurine from hippocampal slices from 3-month-old (adult) and 7-day-old mice were now investigated using a superfusion system. Of group I metabotropic glutamate receptor agonists, quisqualate potentiated basal taurine release in both age groups, more markedly in the immature hippocampus. This action was not antagonized by the specific antagonists of group I but by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione (NBQX), which would suggest an involvement of ionotropic glutamate receptors. (S)-3,5-dihydroxyphenylglycine (DHPG) potentiated the basal release by a receptor-mediated mechanism in the immature hippocampus. The group II agonist (2S, 2′R, 3′R)-2-(2′,3′-dicarboxycyclopropyl)glycine (DCG IV) markedly potentiated basal taurine release at both ages. These effects were antagonized by dizocilpine, indicating again the participation of ionotropic receptors. Group III agonists slightly potentiated basal taurine release, as did several antagonists of the three metabotropic receptor groups. Potassium-stimulated (50 mM K+) taurine release was generally significantly reduced by mGluR agents, mainly by group I and II compounds. This may be harmful to neurons in hyperexcitatory states. On the other hand, the potentiation by mGluRs of basal taurine release, particularly in the immature hippocampus, together with the earlier demonstrated pronounced enhancement by activation of ionotropic glutamate receptors, may protect neurons against excitotoxicity.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 15 (1990), S. 797-804 
    ISSN: 1573-6903
    Keywords: Chloride flux ; GABA ; taurine ; β-alanine ; hypoaurine ; development
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influx of36Cl− was studied in membrane vesicles prepared from different brain regions from 3-day-old and adult mice. In both age groups the influx was enhanced about threefold by γ-aminobutyric acid (GABA), which effect was blocked by bicuculline and picrotoxin but not by baclofen, characteristic of a GABAA receptor-mediated event. In samples from the adult brain stem the GABA stimulation was smaller than in samples from the other brain regions. Most of the compounds studied apparently act at the same receptor site with the following order of efficacy: muscimol 〉 GABA 〉 β-alanine 〉 hypotaurine 〉 taurine. A number of anticonvulsant taurine derivatives were not effective and glycine only in the brain stem. The weak modulatory effects of taurine could be of significance in vivo since depolarizing stimuli release massive amounts of taurine in developing brain tissue.
    Type of Medium: Electronic Resource
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