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首页> 外文期刊>Journal of the Neurological Sciences: Official Bulletin of the World Federation of Neurology >Inhibition of synaptosomal (3H)glutamate uptake and (3H)glutamate binding to plasma membranes from brain of young rats by glutaric acid in vitro.
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Inhibition of synaptosomal (3H)glutamate uptake and (3H)glutamate binding to plasma membranes from brain of young rats by glutaric acid in vitro.

机译：戊二酸在体外抑制幼鼠脑中突触体（3H）谷氨酸的摄取和（3H）谷氨酸与质膜的结合。

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摘要

Synaptosomes and plasma membrane preparations from brain of 30-day-old rats were incubated with glutaric acid at final concentrations ranging from 10 nM to 1 mM for the determination of glutamate uptake and binding, respectively. [3H]Glutamate uptake into synaptosomes was inhibited by approximately 50% by 1 mM glutaric acid, corresponding to the concentration found in brain of glutaric acidemic children. In addition, in the presence of extracellular Na+ concentrations, the same dose of glutaric acid decreased by about 30% [3H]glutamate binding to brain plasma membranes. The results indicate that the inhibition of both glutamate uptake into synaptosomes and glutamate binding to plasma synaptic membranes by the metabolite could result in elevated concentrations of the excitatory neurotransmitter in the synaptic cleft, potentially causing excitotoxicity to neural cells, a fact that may be related to the brain damage characteristic of glutaric acidemia type I.
机译：将来自30日龄大鼠脑的突触小体和质膜制剂与戊二酸孵育，终浓度分别为10 nM至1 mM，以分别测定谷氨酸的摄取和结合。 1 mM戊二酸可抑制[3H]谷氨酸对突触体的吸收，相当于戊二酸血症儿童大脑中的浓度。此外，在细胞外Na +浓度存在的情况下，相同剂量的戊二酸减少了与脑质膜结合的[30H]谷氨酸盐约30％。结果表明，代谢物既抑制谷氨酸摄取到突触体中，又抑制谷氨酸与血浆突触膜结合，可能导致突触间隙中兴奋性神经递质的浓度升高，从而可能对神经细胞造成兴奋性毒性，这一事实可能与I型戊二酸血症的脑损伤特征

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