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  • Title: Endogenous gamma-L-glutamyl and beta-L-aspartyl peptides and excitatory aminoacidergic neurotransmission in the brain.
    Author: Varga V, Janáky R, Saransaari P, Oja SS.
    Journal: Neuropeptides; 1994 Jul; 27(1):19-26. PubMed ID: 7969817.
    Abstract:
    The effects of gamma-L-glutamyl- and beta-L-aspartyl di- and tripeptides on glutamatergic neurotransmission were tested in vitro. Of the peptides, gamma-L-glutamylglutamate was the most effective inhibitor, comparable to glutamate, of both Na(+)-independent and Cl-/Ca(2+)-activated binding/transport of glutamate. gamma-L-glutamylglutamate was most effective in the midbrain and hypothalamus and gamma-L-glutamylaspartate in the hippocampus when tested on the Na(+)-independent binding. The Cl-/Ca(2+)-dependent binding/transport of glutamate was affected by gamma-glutamylaspartate most strongly in the hippocampus. gamma-L-glutamylglycine and beta-L-aspartylglycine moderately inhibited the Na(+)-dependent uptake of L-glutamate and D-aspartate while the other peptides were only weak inhibitors. Reduced and oxidized glutathione enhanced the uptake of L-glutamate. The K(+)-stimulated release of L-glutamate was enhanced by gamma-L-glutamylglutamate and -aspartate and the release of D-aspartate also by gamma-L-glutamylglycine. The results indicate that both pre- and postsynaptic events in glutamatergic neurotransmission are modulated by these endogenous acidic oligopeptides.
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