Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • NO synthase inhibitor  (1)
  • brain synaptosomes  (1)
  • 1
    Electronic Resource
    Electronic Resource
    The use of antioxidants to prevent glutamate-induced derangement of calcium ion metabolism in rat cerebral cortex synaptosomes (2000)
    Springer
    Neuroscience and behavioral physiology 30 (2000), S. 535-541 
    Details
    ISSN: 1573-899X
    Keywords: Glutamate ; calcium ions ; antioxidants ; GM1 ganglioside ; brain synaptosomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Glutamate is shown to induce increases in intracellular Ca2+ concentrations ([Ca2+]i), increases in45Ca2+ influx, decreases in the activity of Na+, K+,-ATPase activity, and activation of the Na+/Ca2+ exchanger in rat cerebral cortex synaptosomes. NMDA receptor antagonists virtually prevented these effects. Preincubation of synaptosomes with α-tocopherol, superoxide dismutase, and ganglioside GM1 normalized [Ca2+]i,45Ca2+, influx, and Na+, K+-ATPase activity in rat cerebral cortex synaptosomes exposed to glutamate. Glutamate and GM1 activated the Na+/K+ exchanger, and their effects were additive. Calcium ions entering cerebral cortex nerve cells via NMDA receptors during exposure to high glutamate concentrations appeared to be only the trigger for the processes activating free-radical reactions. Activation of these reactions led to increases in Ca2+ influx into cells, decreases in Na+, K+-ATPase activity, and significant increases in [Ca2+]i, though this could be prevented by antioxidants and gangliosides.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02462611
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    The Difference in the Effect of Glutamate and NO Synthase Inhibitor on Free Calcium Concentration and Na+,K+-ATPase Activity in Synaptosomes from Various Brain Regions (1999)
    Springer
    Neurochemical research 24 (1999), S. 1101-1106 
    Details
    ISSN: 1573-6903
    Keywords: Free calcium ; Na+,K+-ATPase ; glutamate ; NO synthase inhibitor ; synaptosomes ; brain regions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The significant increase of free calcium concentration ([Ca2+]i) was found in rat cerebral cortex synaptosomes and hippocampal crude synaptosomal fraction after their exposure to glutamate. But no change of [Ca2+]i was revealed in cerebellar synaptosomes, the slight increase of [Ca2+]i in striatal synaptosomes was not significant. The presence of Ng-nitro-L-arginine methyl ester (L-NAME) in the incubation medium practically prevented the increase of [Ca2+]i initiated by glutamate in cerebral cortex synaptosomes, but not in hippocampal ones. The significant diminution of [Ca2+]i in the presence of this inhibitor was shown in striatal synaptosomes exposed to glutamate. Na+,K+-ATPase activity is significantly lower in cerebral cortex, striatal and hippocampal synaptosomes exposed to glutamate. L-NAME prevented the inactivation of this enzyme by glutamate. In cerebellar synaptosomes the tendency to the decrease of enzymatic activity in the presence of L-NAME was on the contrary noticed. Thus, the data obtained provide evidence of the protective effect of NO synthase inhibitor in brain cortex and striatal synaptosomes, but not in cerebellar synaptosomes. Synaptosomes appear to be an adequate model to study the regional differences in the mechanism of toxic effect of excitatory amino acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020752101736
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...