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  • 1
    Electronic Resource
    Electronic Resource
    Release of Endogenous Taurine and γ-Aminobutyric Acid from Brain Slices from the Adult and Developing Mouse (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The spontaneous and potassium-stimulated release of endogenous taurine and γ-aminobutyric acid (GABA) from cerebral cortex and cerebellum slices from adult and developing mice was studied in a superfusion system. The spontaneous release of GABA was of the same magnitude in slices from adult and developing mice, but the spontaneous release of taurine was considerably greater in the adults. The potassium-stimulated release of GABA from cerebral cortex slices was about five times greater in adult than in 3-day-old mice, but the potassium-stimulated release of taurine was more than six times greater in 3-day-old than in adult mice. In cerebellar slices from 7-day-old mice, potassium stimulation also evoked a massive release of taurine, whereas the evoked release from slices from adult mice was rather negligible. Also in cerebellar slices the potassium-stimulated release of GABA exhibited the opposite quantitative pattern. The stimulated release of both GABA and taurine was partially calcium dependent. The results suggest that taurine may be an important regulator of excitability in the developing brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb01842.x
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  • 2
    Electronic Resource
    Electronic Resource
    Taurine and GABA release from mouse cerebral cortex slices: Effects of structural analogues and drugs (1987)
    Springer
    Neurochemical research 12 (1987), S. 475-482 
    Details
    ISSN: 1573-6903
    Keywords: Brain slices ; taurine ; GABA ; release ; structural analogues ; drugs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of structural analogues, excitatory amino acids and certain drugs on spontaneous and potassium-stimulated exogenous taurine and GABA release were investigated in mouse cerebral cortex slices using a superfusion system. Spontaneous efflux of both amino acids was rather slow but could be enhanced by their uptake inhibitors. Taurine efflux was facilitated by exogenous taurine, hypotaurine, β-alanine and GABA, whereas GABA, nipecotic acid and homotaurine effectively enhanced GABA release. The stimulatory potency of the analogues closely corresponded to their ability to inhibit taurine and GABA uptake, respectively, indicating that these efflux processes could be mediated by the carriers operating outwards. Glutamate induced GABA release, whereas taurine efflux was potentiated by aspartate, glutamate, cysteate, homocysteate and kainate. The centrally acting drugs, including GABA agonists and antagonists, as well as the proposed taurine antagonist TAG (6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide), had no marked effects on spontaneous taurine and GABA release. Potassium ions stimulated dosedependently both taurine and GABA release from the slices, the responses of taurine being strikingly slow but sustained. Exogenous GABA and nipecotic acid accelerated the potassium-stimulated GABA release, whereas picrotoxin and bicuculline were ineffective. The potassium-stimulated taurine release was unaltered or suppressed by exogenous taurine and analogues, differing in this respect from GABA release. The apparent magnitude of the depolarization-induced GABA release is thus influenced by the function of membrane transport sites, but the same conclusion cannot be drawn with regard to taurine. Haloperidol and imipramine were able to affect the evoked release of both taurine and GABA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00972301
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  • 3
    Electronic Resource
    Electronic Resource
    Mechanisms of D-Aspartate Release Under Ischemic Conditions in Mouse Hippocampal Slices (1999)
    Springer
    Neurochemical research 24 (1999), S. 1009-1016 
    Details
    ISSN: 1573-6903
    Keywords: D-aspartate release ; hippocampal slices ; ischemia ; cell-damaging conditions ; metabolic poisons ; mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The release of preloaded D-[3H]aspartate, an unmetabolizable analogue of L-glutamate, was studied in superfused hippocampal slices from 7-day-old and 3-month-old (adult) mice under various cell-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress and the presence of free radicals and metabolic poisons. The release was generally markedly enhanced in most of the above conditions, the responses being greater in adults than in developing mice. The presence of dinitrophenol had the most pronounced effect at both ages, followed by NaCN- and free-radical-containing media and ischemia. Hypoxia did not affect release in the immature hippocampus. Under most conditions K+ stimulation (50 mM) was still able markedly to enhance D-aspartate release. This potentiation under cell-damaging conditions in both adult and developing hippocampus signifies that increased L-glutamate release contributes to excitotoxicity and subsequent cell death. The mechanisms of ischemia-induced release of D-aspartate were analyzed in the adult hippocampus using ion channel inhibitors and modified superfusion media. The induced release proved to be partly Ca2+-dependent and partly Ca2+-independent. The results obtained with Na+ omission and homo- and heteroexchange with D-aspartate and L-glutamate demonstrated that a part of the release in normoxia and ischemia is mediated by the reversal of Na+-dependent glutamate transporters. The Na+ channel blockers amiloride and riluzole reduced the ischemia-induced release, also indicating the involvement of Na+ channels. In addition to this, the enhanced release of D-aspartate may comprise a swelling-induced component through chloride channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1021052725921
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  • 4
    Electronic Resource
    Electronic Resource
    Modulation of GABAergic neurotransmission in the brain by dipeptides (1988)
    Springer
    Neurochemical research 13 (1988), S. 1027-1034 
    Details
    ISSN: 1573-6903
    Keywords: Neurotransmission ; GABA ; dipeptides ; chloride flux
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of endogenous and synthetic peptides containing GABA or its analogues on the GABA/benzodiazepine/chloride ionophore, complex, GABAB receptor, Cl fluxes, GABA release and GABA uptake were studied using synaptic membranes, crude synaptoneurosomal preparations and slices prepared from the rat and mouse brain. The sodium-independent binding of GABA was strongly inhibited by GABA-histidine, followed by γ-glutamyl-homotaurine, GABA-glycine and γ-glutamyl-GABA. The binding of diazepam was slightly enhanced by the same peptides. The peptides alone had no effect on the chloride fluxes, but GABA-histidine, γ-glutamyl-GABA and GABA-glycine enhanced while γ-glutamyl-homotaurine and GABA-taurine inhibited GABA-stimulated chloride uptake. GABA-histidine was the most effective displacer of baclofen binding, but γ-glutamyl-homotaurine was entirely ineffective. The uptake of GABA was markedly inhibited in synaptosomal preparations by GABA-histidine, while all other peptides were less effective. γ-Glutamyl-taurine attenuated but γ-glutamyl-homotaurine and GABA-glycine enhanced the potassium-stimulated release of GABA. The present actions of GABA-histidine in vitro may be of significance for GABAergic neurotransmission in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00973146
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  • 5
    Electronic Resource
    Electronic Resource
    Interference of S-Alkyl Derivatives of Glutathione with Brain Ionotropic Glutamate Receptors (1998)
    Springer
    Neurochemical research 23 (1998), S. 1085-1091 
    Details
    ISSN: 1573-6903
    Keywords: Glutamate receptors ; glutathione derivatives ; ligand binding ; Ca2+ influx
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of glutathione, glutathione sulfonate and S-alkyl derivatives of glutathione on the binding of glutamate and selective ligands of ionotropic N-methyl-D-aspartate (NMDA) and non-NMDA receptors were studied with mouse synaptic membranes. The effects of glutathione and its analogues on 45Ca2+ influx were also estimated in cultured rat cerebellar granule cells. Reduced and oxidized glutathione, glutathione sulfonate, S-methyl-, -ethyl-, -propyl-, -butyl- and -pentylglutathione inhibited the Na+-independent binding of L-[3H]glutamate. They strongly inhibited also the binding of (S)-2-amino-3-hydroxy-5-[3H]methyl-4-isoxazolepropionate [3H]AMPA (IC50 values: 0.8–15.9 μM). S-Alkylation of glutathione rendered the derivatives unable to inhibit [3H]kainate binding. The NMDA-sensitive binding of L-[3H]glutamate and the binding of 3-[(R)-2-carboxypiperazin-4-yl][1,2-3H]propyl-1-phosphonate ([3H]CPP, a competitive antagonist at NMDA sites) were inhibited by the peptides at micromolar concentrations. The strychnine-insensitive binding of the NMDA coagonist [3H]glycine was attenuated only by oxidized glutathione and glutathione sulfonate. All peptides slightly enhanced the use-dependent binding of [3H]dizocilpine (MK-801) to the NMDA-gated ionophores. This effect was additive with the effect of glycine but not with that of saturating concentrations of glutamate or glutamate plus glycine. The glutamate- and NMDA-evoked influx of 45Ca2+ into cerebellar granule cells was inhibited by the S-alkyl derivatives of glutathione. We conclude that besides glutathione the endogenous S-methylglutathione and glutathione sulfonate and the synthetic S-alkyl derivatives of glutathione act as ligands of the AMPA and NMDA receptors. In the NMDA receptor-ionophore these glutathione analogues bind preferably to the glutamate recognition site via their γ-glutamyl moieties.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020712203611
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  • 6
    Electronic Resource
    Electronic Resource
    β-Alanine Release from the Adult and Developing Hippocampus Is Enhanced by Ionotropic Glutamate Receptor Agonists and Cell-Damaging Conditions (1999)
    Springer
    Neurochemical research 24 (1999), S. 407-414 
    Details
    ISSN: 1573-6903
    Keywords: β-Alanine release ; hippocampal slices ; glutamate agonists ; cell-damaging conditions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The release of the inhibitory amino acid β-alanine was investigated in hippocampal slices from adult (3-month-old) and developing (7-day-old) mice, using a superfusion system. The release was enhanced by β-alanine itself and the structural analogs taurine and γ-aminobutyrate. It was dependent on Na+, but independent of Ca2+ in both mature and immature hippocampus, being thus mostly mediated by uptake carriers operating in an outward direction. The release was potentiated in the developing mice, but not affected in the adults, by the ionotropic glutamate receptor agonists N-methyl-D-aspartate, kainate, 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and tetrazolylglycine in a receptor-mediated manner. Cell-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress and the presence of free radicals, greatly enhanced β-alanine release at both ages, but more markedly in the adults. The great amounts of β-alanine, together with the inhibitory amino acids taurine and γ-aminobutyrate, released simultaneously with the excitatory amino acids in the hippocampus may constitute an important protective mechanism against excitotoxicity, which leads to neuronal death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020941818168
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  • 7
    Electronic Resource
    Electronic Resource
    Lamotrigine and Carbamazepine Affect Differently the Release of D-[3H]Aspartate from Mouse Cerebral Cortex Slices: Involvement of NO (1999)
    Springer
    Neurochemical research 24 (1999), S. 1153-1159 
    Details
    ISSN: 1573-6903
    Keywords: Lamotrigine ; carbamazepine ; D-aspartate release ; veratridine ; potassium stimulation ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of lamotrigine and carbamazepine on the release of preloaded D-[3H]aspartate and the involvement of nitric oxide were studied with mouse cerebral cortical slices in a superfusion system. Lamotrigine inhibited the veratridine-evoked release, whereas the K+-stimulated release was attenuated more strongly by carbamazepine than by lamotrigine. These effects were accentuated by the N-methyl-D-aspartate receptor antagonist L-2-amino-5-phosphonovalerate and the nitric oxide synthase inhibitor L-nitroarginine, but diminished by the nitric oxide donor sodium nitroprusside. The results show that in addition to the blockade of voltage-sensitive Na+ (and Ca2+) channels, NO-mediated mechanisms are probably involved in the anticonvulsant actions of carbamazepine and, in particular, those of lamotrigine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020716621300
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  • 8
    Electronic Resource
    Electronic Resource
    Enhanced GABA release in cerebral cortical slices derived from rats with thioacetamide-induced hepatic encephalopathy (1992)
    Springer
    Neurochemical research 17 (1992), S. 1187-1190 
    Details
    ISSN: 1573-6903
    Keywords: Hepatic encephalopathy ; thioacetamide ; cerebral cortex ; GABA release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The release of newly loaded [3H]GABA was studied in slices of different brain regions derived from rats in which acute hepatic encephalopathy (HE) was induced with a hepatotoxin thioacetamide. HE increased both spontaneous and high (50 mM) ammonium chloride-evoked GABA release in cerebral cortical slices by 38% and 50%, respectively. No effects of HE were noted in cerebellar or striatal slices. An increased release of GABA in the cerebral cortex may contribute to the endogenous benzodiazepine-mediated enhancement of GABAergic tone, which is thought to be partly responsible for the pathophysiological mechanism of HE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00968397
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  • 9
    Electronic Resource
    Electronic Resource
    Taurine in the developing cat: Uptake and release in different brain areas (1994)
    Springer
    Neurochemical research 19 (1994), S. 77-82 
    Details
    ISSN: 1573-6903
    Keywords: Taurine ; uptake ; release ; cat brain slices ; synaptosomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Taurine is an important modulator of neuronal activity in the immature brain. In kittens, taurine deficiency causes serious dysfunction in the cerebellar and cerebral visual cortex. The processes of taurine transport in vitro were now studied for the first time in different brain areas in developing and adult cats. The uptake of taurine consisted initially of two saturable components, high- and low-affinity, in synaptosomal preparations from the developing cerebral cortex and cerebellum, but the high-affinity uptake component completely disappeared during maturation. The release of both endogenous and preloaded labeled taurine from brain slices measured in a superfusion system was severalfold stimulated with a slow onset by depolarizing K+ (50 mM) concentrations. K+ stimulation released markedly more taurine from the cerebral cortex, cerebellum and brain stem in kittens than in adult cats. The responses were largest in the cerebellum. Both uptake and release of taurine are thus highly efficient in the brain of kittens and may be of significance in view of the vulnerability of cats to taurine deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00966732
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  • 10
    Electronic Resource
    Electronic Resource
    Release of [3H]Dopamine from Striatal and Cerebral Cortical Slices from Rats with Thioacetamide-Induced Hepatic Encephalopathy: Different Responses to Stimulation by Potassium Ions and Agonists of Ionotropic Glutamate Receptors (1997)
    Springer
    Neurochemical research 22 (1997), S. 101-106 
    Details
    ISSN: 1573-6903
    Keywords: Hepatic encephalopathy ; brain slices ; striatum ; frontal cortex ; glutamate receptors ; dopamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of depolarizing stimuli; high (50 mM) potassium ions and the glutamate receptor agonists N-methyl-D-aspartate, kainate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) on the release of newly-loaded [3H]dopamine were studied in frontal cortical and striatal slices from control rats and from rats with acute hepatic encephalopathy induced with a hepatotoxin, thioacetamide. Hepatic encephalopathy enhanced the stimulatory effect of potassium ions by 20% in striatal slices and by 34% in frontal cortical slices. In striatal slices the stimulatory effects of N-methyl-D-aspartate and kainate were depressed in hepatic encephalopathy by 46% and 21%, respectively, which may be taken to reflect impaired modulation of striatal dopamine release by glutamate acting at N-methyl-D-aspartate or kainate receptors. In frontal cortical slices, the stimulatory effect of kainate was enhanced by 35% in hepatic encephalopathy but N-methyl-D-aspartate-stimulated release was not affected. The release evoked by 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate was not affected in hepatic encephalopathy in either brain region. Stimulation of dopamine release in the frontal cortex by depolarization or glutamate acting at kainate receptors could inhibit the activity of descending corticostriatal glutamatergic pathways, further impairing regulation of dopamine release by glutamate in the stratum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027347019707
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