肌萎缩侧索硬化
谷氨酸受体
神经科学
兴奋毒性
抑制性突触后电位
致电离效应
化学
NMDA受体
兴奋性突触后电位
甘氨酸
利鲁唑
内生
生物
生物化学
受体
氨基酸
医学
内科学
疾病
作者
Jumpei Sasabe,Sadakazu Aiso
标识
DOI:10.1002/cbdv.200900306
摘要
The mechanism underlying selective motoneuronal loss in amyotrophic lateral sclerosis (ALS) remains uncertain. The pathogenesis appears to be a complex and multifactorial process. Glutamate excitotoxicity to motoneuron is one of the most intensely investigated targets for the treatment of ALS, and excessive motoneuronal excitation by glutamate through ionotropic glutamate receptors has been mainly demonstrated. However, development of clinically effective drug targeting glutamate is sometimes difficult, because some aspects of glutamergic signals also could be beneficial, as the injured neurons attempt to recruit endogenous recovery. This review is focused on identifying other mechanisms of imbalanced excitation in ALS motoneurons including excitation-modulating D-serine and inhibitory glycine/GABA. Further, validation of these mechanisms might ultimately lead us to new therapeutic targets for ALS.
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