BOAA selectively enhances L-glutamate release from guinea pig hippocampal mossy fiber synaptosomes.

The neurotoxic amino acids beta-N-oxalylamino-L-alanine (BOAA) and beta-N-methylamino-L-alanine (BMAA) were evaluated for possible effects on spontaneous and stimulus-evoked release of L-glutamate (L-Glu) and dynorphin A(1-8)-like immunoreactivity (LI) from guinea pig hippocampal mossy fiber synaptosomes. BOAA (200 microM), but not BMAA (1 mM), was found to significantly increase both basal cytosolic and KCl-stimulated vesicular release of L-Glu. Neither BOAA nor BMAA had any effect on dynorphin A(1-8)-LI release from these synaptosomes. This is the first report describing a presynaptic facilitatory action of BOAA upon L-Glu release; an effect which may contribute to the neurotoxic properties of this proposed environmental toxin.