BOAA可选择性增强豚鼠海马苔藓纤维突触体中L-谷氨酸的释放。

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

作者信息

Gannon R L, Terrian D M

机构信息

Clinical Sciences Division, USAF School of Aerospace Medicine, Brooks AFB, TX 78235-5301.

出版信息

Neurosci Lett. 1989 Dec 15;107(1-3):289-94. doi: 10.1016/0304-3940(89)90833-1.

DOI:10.1016/0304-3940(89)90833-1

PMID:2575728

Abstract

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.

摘要

对神经毒性氨基酸β-N-草酰氨基-L-丙氨酸（BOAA）和β-N-甲基氨基-L-丙氨酸（BMAA）进行了评估，以研究它们对豚鼠海马苔藓纤维突触体中L-谷氨酸（L-Glu）的自发释放和刺激诱发释放以及强啡肽A（1-8）样免疫反应性（LI）的可能影响。发现BOAA（200微摩尔）而非BMAA（1毫摩尔）能显著增加L-Glu的基础胞质释放和KCl刺激的囊泡释放。BOAA和BMAA对这些突触体中强啡肽A（1-8）-LI的释放均无影响。这是首次报道BOAA对L-Glu释放具有突触前促进作用；该作用可能有助于这种潜在环境毒素的神经毒性特性。