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Hydrogen Peroxide Induces a Long‐Lasting Inhibition of the Ca 2+ ‐Dependent Glutamate Release in Cerebrocortical Synaptosomes Without Interfering with Cytosolic Ca 2+
Author(s) -
Zoccarato Franco,
Valente Marina,
Alexandre Adolfo
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64062552.x
Subject(s) - exocytosis , chemistry , ionomycin , synaptosome , glutamate receptor , phosphocreatine , biophysics , biochemistry , endocrinology , intracellular , biology , membrane , energy metabolism , receptor
We studied the action of H 2 O 2 on the exocytosis of glutamate by cerebrocortical synaptosomes. The treatment of synaptosomes with H 2 O 2 (50–150 µ M ) for a few minutes results in a long‐lasting depression of the Ca 2+ ‐dependent exocytosis of glutamate, induced by KCl or by the K + ‐channel inhibitor 4‐aminopyridine. The energy state of synaptosomes, as judged by the level of phosphocreatine and the ATP/ADP ratio, was not affected by H 2 O 2 , although a transient decrease was observed after the treatment. H 2 O 2 did not promote peroxidation, as judged by the formation of malondialdehyde. In indo‐1‐loaded synaptosomes, the treatment with H 2 O 2 did not modify significantly the KCl‐induced increase of [Ca 2+ ] i . H 2 O 2 inhibited exocytosis also when the latter was induced by increasing [Ca 2+ ] i with the Ca 2+ ionophore ionomycin. The effects of H 2 O 2 were unchanged in the presence of superoxide dismutase and the presence of the Fe 3+ chelator deferoxamine. These results appear to indicate that H 2 O 2 , apparently without damaging the synaptosomes, induces a long‐lasting inhibition of the exocytosis of glutamate by acting directly on the exocytotic process.