Abstract
The neurotoxic amino acids β-N- oxalylamino- l-alanine (BOAA) and β-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 μM), but not BMAA (1 mM), was found to significantly increase both basal cytosolic and KC1-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.
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