Recent literature demonstrated that exposure to excitatory amino acid in specific experimental conditions might produce a defect in the autophagy pathway. Such an effect was observed in motor neurons exposed chronically to glutamate agonists. On the other hand, it is well known that glutamate induces motor neuron death and this is supposed to play a key role in the physiopathology of motor neuron loss in amyotrophic lateral sclerosis (ALS). Similarly, a defective recruitment of autophagy was recently documented in ALS. In the present study we found that exposure of motor neurons to kainic acid produces intracellular changes associated with defective autophagy. In this experimental conditions, pharmacological activation of autophagy rescues the loss of motor neurons.

中文翻译：

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谷氨酸诱导的运动神经元丢失的自噬激活。

最近的文献表明在特定的实验条件下暴露于兴奋性氨基酸可能会导致自噬途径的缺陷。在长期暴露于谷氨酸激动剂的运动神经元中观察到了这种作用。另一方面，众所周知谷氨酸诱导运动神经元死亡，这被认为在肌萎缩性侧索硬化症（ALS）中运动神经元丢失的生理病理学中起关键作用。同样，最近在ALS中发现自噬的募集有缺陷。在本研究中，我们发现运动神经元暴露于海藻酸会产生与自噬缺陷有关的细胞内变化。在这种实验条件下，自噬的药理激活可以挽救运动神经元的丢失。