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  • 1
    Electronic Resource
    Electronic Resource
    Anion Conductance Blocked by Divalent Cations in Cultured Rat Astrocytes (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 633 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb15669.x
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  • 2
    Electronic Resource
    Electronic Resource
    Interactions of γ-L-glutamyltaurine with excitatory aminoacidergic neurotransmission (1994)
    Springer
    Neurochemical research 19 (1994), S. 243-248 
    Details
    ISSN: 1573-6903
    Keywords: Glutamate neurotransmission ; taurine peptides ; neuromodulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The in vitro effects of γ-L-glutamyltaurine on different stages of excitatory aminoacidergic neurotransmission were tested with γ-D-glutamyltaurine as reference. γ-L-Glutamyltaurine enhanced the K+-stimulated release of [3H]glutamate from cerebral cortical slices (25% at 0.1 mM) and slightly inhibited the uptake by crude brain synaptosomal preparations (about 10% at 1 mM). γ-L-Glutamyltaurine was also a weak displacer of glutamate and its agonists from their binding sites in brain synaptic membrane preparations, being, however, less selective to quisqualate (QA) sites than γ-D-glutamyltaurine. The basal influx of Ca2+ into cultured cerebellar granular cells was not affected by 1 mM γ-L-glutamyltaurine, but the glutamate- and its agonist-activated influx was significantly inhibited in low-Mg2+ (0.1 mM) and Mg2+-free media. The glutamate-evoked increase in free intracellular Ca2+ and the kainate-activated formation of cGMP in cerebellar slices were both markedly inhibited by 0.1 mM γ-L-giutamyltaurine. We propose that γ-L-glutamyltaurine may act as endogenous modulator in excitatory aminoacidergic neurotransmission.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00971571
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  • 3
    Electronic Resource
    Electronic Resource
    Glutamate agonists and [3H]GABA release from rat hippocampal slices: Involvement of metabotropic glutamate receptors in the quisqualate-evoked release (1994)
    Springer
    Neurochemical research 19 (1994), S. 729-734 
    Details
    ISSN: 1573-6903
    Keywords: GABA release ; quisqualate ; glutamate receptors ; metabotropic receptors ; hippocampal slices
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of glutamate agonists and their selective antagonists on the Ca2+-dependent and independent releases of [3H]GABA from rat coronal hippocampal slices were studied in a superfusion system. The Ca2+-dependent release evoked by glutamate, kainate and N-methyl-D-aspartate (NMDA) gradually declined with time despite the continuous presence of the agonists. Quisqualate (QA) caused a sustained release which exhibited no tendency to decline within the 20-min period of stimulation. This release was enhanced in Ca2+-free medium. The release evoked by QA in Ca2+-containing medium was significantly inhibited by (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohept-5,10-imine hydrogen maleate (MK-801) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), showing that QA activates NMDA receptors directly or indirectly through (RS)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors. The inhibition of MK-801 was slightly diminished and that of CNQX totally abolished in Ca2+-free medium. Verapamil inhibited the QA-activated release in both Ca2+-containing and Ca2+-free media. The effect of QA but not that of AMPA was blocked in Ca2+-free medium by L(+)-2-amino-3-phosphonopropionate (L-AP3), a selective antagonist of the metabotropic glutamate receptor. It is suggested that the sustained release of GABA is also mediated partly by activation of metabotropic receptors and mobilization of Ca2+ from intracellular stores.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00967713
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of magnesium on calcium influx activated by glutamate and its agonists in cultured cerebellar granule cells (1992)
    Springer
    Neurochemical research 17 (1992), S. 1195-1200 
    Details
    ISSN: 1573-6903
    Keywords: Calcium influx ; cultured cerebellar granule cells ; glutamate ; kainate ; quisqualate ; magnesium ions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of Mg2+ on the glutamate-, kainate-, N-methyl-d-aspartate- and quisqualate-induced influx of45Ca2+ were studied in cultured cerebellar granule cells. The N-methyl-d-aspartate- and quisqualate-evoked influx was totally and the kainate- and glutamate-evoked influx partially blocked in 1.3 mM extracellular Mg2+. The increase in influx induced by kainate, quisqualate and glutamate was maximal at 0.1 mM Mg2+, whereas N-methyl-d-aspartate was most effective in totally Mg2+-free media.d-2-Amino-5-phosphonovalerate blocked partially and phencyclidine completely the enhancement of Ca2+ influx by 1 mM quisqualate in 0.1-mM Mg2+ medium. The effect of 10 μM quisqualate was also significantly inhibited by antagonists specific for different glutamate receptor subtypes, including N-methyl-d-aspartate, (RS)α-amino-3-hydroxy-5-methyl-4-isozazolepropionate and metabotropic recptors. This evidences a heterogeneous action of quisqualate, mediated by different glutamate receptor subtypes in 0.1 mM Mg2+ medium. The efficacy of quisqualate in inducing influx of Ca+ and the selectivity of antagonists for different receptors are also modified by extracellular Mg2+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00968399
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    Paper (German National Licenses)
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