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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Cholesterol depletion attenuates tonic release but increases the ambient level of glutamate in rat brain synaptosomes.
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Cholesterol depletion attenuates tonic release but increases the ambient level of glutamate in rat brain synaptosomes.

机译：胆固醇的消耗减弱了滋补剂的释放，但增加了大鼠脑突触小体中谷氨酸的环境水平。

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摘要

The low level of ambient glutamate is important for the brain's spontaneous activity and proper synaptic transmission. Cholesterol deficiency has been implicated in the pathogenesis of several neurodegenerative disorders. It was examined whether membrane cholesterol modulated the extracellular glutamate level in nerve terminals and the processes responsible for its maintenance. The ambient L-[(14)C]glutamate level, being an equilibrium between Na(+)-dependent uptake and tonic release, was increased from 0.193+/-0.013 nmol/mg protein to 0.282+/-0.013 (extracellular endogenous glutamate-from 6.9+/-2.0 to 16.6+/-2.0, respectively) in rat brain synaptosomes treated with a cholesterol acceptor methyl-beta-cyclodextrin (MbetaCD). This alteration was not due to the change in the activity of glutamine synthetase that was shown with the specific blocker L-methionine sulfoximine. In the presence of DL-threo-beta-benzyloxyaspartate, which significantly reduced the contribution of glutamate transporters, net tonic release of L-[(14)C]glutamate was decreased by 38% and release in low-Na(+) medium was attenuated by 41% after cholesterol extraction. Also, cholesterol-deficient synaptosomes showed a reduced content of cytosolic L-[(14)C]glutamate and a lower initial velocity of L-[(14)C]glutamate uptake. We suggested that cholesterol deficiency altered the intra-to-extracellular glutamate ratio by the reduction of the cytosolic level of the neurotransmitter and the augmentation of the ambient glutamate level, thereby favoring a decrease in tonic glutamate release. Thus, increased extracellular glutamate in cholesterol-deficient nerve terminals was not a result of the changes in tonic release and/or glutamine synthetase activity, but was set by lack function of glutamate transporters.
机译：低水平的环境谷氨酸对于大脑的自发活动和正确的突触传递很重要。胆固醇缺乏与几种神经退行性疾病的发病机理有关。检查了膜胆固醇是否调节了神经末梢中细胞外谷氨酸的水平及其维持过程。周围的L-[（14）C]谷氨酸水平是Na（+）依赖性摄取和补品释放之间的平衡，从0.193 +/- 0.013 nmol / mg蛋白质增加到0.282 +/- 0.013（细胞外内源性谷氨酸-在分别用胆固醇受体甲基-β-环糊精（MbetaCD）处理的大鼠脑突触小体中-（分别从6.9 +/- 2.0到16.6 +/- 2.0）。这种改变不是由于用特定的阻滞剂L-甲硫氨酸亚砜肟显示的谷氨酰胺合成酶活性的变化。在DL-苏-β-苄氧基天冬氨酸的存在下，这大大降低了谷氨酸转运蛋白的贡献，L-[（14）C]谷氨酸的净补品释放减少了38％，在低Na（+）培养基中的释放是胆固醇提取后减少41％。同样，缺乏胆固醇的突触体显示出降低的胞质L-[（14）C]谷氨酸含量和较低的L-[（14）C]谷氨酸初始摄取速度。我们建议胆固醇缺乏症通过降低神经递质的胞质水平和增加周围谷氨酸水平来改变细胞内谷氨酸比例，从而有利于降低补品谷氨酸的释放。因此，胆固醇缺乏的神经末梢中细胞外谷氨酸的增加不是滋补释放和/或谷氨酰胺合成酶活性变化的结果，而是由谷氨酸转运蛋白缺乏的功能引起的。

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