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Characterization of the Effect of Monensin on γ‐Amino‐ n ‐Butyric Acid Release from Isolated Nerve Terminals
Author(s) -
Sitges María
Publication year - 1989
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 - 10.1111/j.1471-4159.1989.tb07354.x
Subject(s) - monensin , ionophore , chemistry , butyric acid , biophysics , efflux , neurotransmitter , tetrodotoxin , synaptosome , amino acid , biochemistry , membrane , biology , receptor
The action of the polyether antibiotic monensin on the release of γ‐[ 3 H]amino‐ n ‐butyric acid ([ 3 H]GABA) from mouse brain synaptosomes is characterized. Monensin enhances the release of this amino acid transmitter in a dose‐dependent manner and does not modify the efflux of the nontransmitter amino acid α‐[ 3 H]aminoisobMtyrate. The absence of external Ca 2+ fails to prevent the stimulatory effect of monensin on [ 3 H]GABA release. Furthermore, monensin is less effective in stimulating [ 3 H]GABA release in the presence of Ca 2+ . The releasing response to monensin is absolutely dependent on external Na + . The blockade of voltage‐sensitive Na + or Ca 2+ channels does not modify monensin‐induced release of the transmitter. Also, the blockade of the GABA uptake pathway fails to prevent the stimulatory effect of monensin on [ 3 H]GABA release. Although monensin markedly increases Na + permeability in synaptosomes, these data indicate that the Ca 2+ ‐independent monensin‐stimulated transmitter release is not mediated by the Na + ‐dependent uptake pathway. It is concluded that the entrance of Na + through monensin molecules inserted in the presynaptic membrane might be sufficient to initiate the intraterminal molecular events underlying transmitter release.