These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Modulation of glutamate agonist-induced influx of calcium into neurons by gamma-L-glutamyl and beta-L-aspartyl dipeptides.
    Author: Varga V, Janáky R, Oja SS.
    Journal: Neurosci Lett; 1992 Apr 27; 138(2):270-4. PubMed ID: 1351662.
    Abstract:
    Gamma-L-Glutamate and beta-L-aspartate dipeptides, present in the mammalian brain with a yet unknown function, were shown to affect the influx of Ca2+ into cultured cerebellar granule cells. The most active peptides, gamma-L-glutamyl-L-aspartate, gamma-L-glutamyl-L-glutamate and gamma-L-glutamylglycine, enhanced the basal influx but inhibited the glutamate-activated influx of Ca2+ in a dose-dependent manner. Gamma-L-Glutamyl-L-aspartate, the strongest inhibitor of the glutamate-activated influx of Ca2+, exhibited selective Mg(2+)-dependent antagonism in the N-methyl-D-aspartate (NMDA)-activated influx of Ca2+. This finding may explain its previously shown deleterious effects on the long-term memory. On the other hand, gamma-L-glutamyl-L-aspartate enhanced alone the entry of Ca2+ into neurons. This effect was antagonized by the non-NMDA antagonists 6-nitro-7-cyanoquinoxaline-2,3-dione (CNQX) and 6,7-dinitroquinoxaline-2,3-dione (DNQX), suggesting a non-NMDA receptor-mediated action, that may also be involved in excitotoxicity in some neurodegenerative disorders.
    [Abstract] [Full Text] [Related] [New Search]