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  • Glutamate neurotransmission  (1)
  • Glutamate receptors  (1)
  • N-methyl-D-aspartate receptors  (1)
  • Titanium  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Titanium-magnesium complexes containing perpendicularly bridging bis(trimethylsilyl) acetylene ligands
    Amsterdam : Elsevier
    Journal of Organometallic Chemistry 475 (1994), S. 127-137 
    Details
    ISSN: 0022-328X
    Keywords: Bis(trimethylsilyl)acetylene ; Bridging ligand ; Magnesium ; Titanium ; X-ray structure
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0022-328X(94)84015-6
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Glutathione Is an Endogenous Ligand of Rat Brain N-Methyl-D-Aspartate (NMDA) and 2-Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionate (AMPA) Receptors (1997)
    Springer
    Neurochemical research 22 (1997), S. 1165-1171 
    Details
    ISSN: 1573-6903
    Keywords: Glutamate receptors ; endogenous regulator ; reduced and oxidized glutathione
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A study was made of the effects of reduced (GSH) and oxidized (GSSG) glutathione on the Na+-independent and N-methyl-D-aspartate (NMDA) displaceable bindings of glutamate, on the binding of kainate, 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), and ligands of the brain NMDA receptor-ionophore complex: glycine, dizocilpine (MK-801) and (±)-3-(2-car-boxypiperazin-4-yl)propyl-1-phosphonate (CPP). GSH and GSSG strongly inhibited the binding of glutamate, CPP and AMPA, kainate and glycine binding being less affected. Both peptides enhanced the binding of dizocilpine in a time- and concentration-dependent manner. This activatory effect was not additive to that of saturating concentrations of glutamate or glutamate plus glycine. The activation of dizocilpine binding by GSH and GSSG was prevented by the competitive NMDA and glycine antagonists DL-2-amino-5-phosphonovalerate and 7-chlorokynurenate. GSH and GSSG may be endogenous ligands of AMPA and NMDA receptors, binding preferably to the glutamate recognition site via their γ-glutamyl moieties. In addition to this, at millimolar concentrations they may regulate the redox state of the NMDA receptor-ionophore complex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027377605054
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    Paper (German National Licenses)
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  • 3
    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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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Mechanisms of L-Cysteine Neurotoxicity (2000)
    Springer
    Neurochemical research 25 (2000), S. 1397-1405 
    Details
    ISSN: 1573-6903
    Keywords: L-Cysteine ; neurotoxicity ; N-methyl-D-aspartate receptors ; free radicals ; catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We review here the possible mechanisms of neuronal degeneration caused by L-cysteine, an odd excitotoxin. L-Cysteine lacks the omega carboxyl group required for excitotoxic actions via excitatory amino acid receptors, yet it evokes N-methyl-D-aspartate (NMDA) -like excitotoxic neuronal death and potentiates the Ca2+ influx evoked by NMDA. Both actions are prevented by NMDA antagonists. One target for cysteine effects is thus the NMDA receptor. The following mechanisms are discussed now: (1) possible increase in extracellular glutamate via release or inhibition of uptake/degradation, (2) generation of cysteine α-carbamate, a toxic analog of NMDA, (3) generation of toxic oxidized cysteine derivatives, (4) chelation of Zn2+ which blocks the NMDA receptor-ionophore, (5) direct interaction with the NMDA receptor redox site(s), (6) generation of free radicals, and (7) formation of S-nitrosocysteine. In addition to these, we describe another new alternative for cytotoxicity: (8) generation of the neurotoxic catecholamine derivative, 5-S-cysteinyl-3,4-dihydroxyphenylacetate (cysdopac).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007616817499
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    Paper (German National Licenses)
    Fulltext
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