自噬
肌萎缩侧索硬化
谷氨酸受体
运动神经元
红藻氨酸
神经科学
神经元
兴奋性突触后电位
化学
生物
生物化学
医学
内科学
抑制性突触后电位
脊髓
细胞凋亡
受体
疾病
作者
Federica Fulceri,Michela Ferrucci,Gloria Lazzeri,Silvio Paparelli,Alessia Bartalucci,Ilaria Tamburini,Antonio Paparelli,Francesco Fornai
出处
期刊:PubMed
日期:2011-03-01
卷期号:149 (1): 101-11
被引量:16
标识
DOI:10.4449/aib.v149i1.1259
摘要
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.
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