AMPA受体
神经传递
神经科学
癫痫
跨膜蛋白
海马结构
生物
突触后密度
受体
化学
突触可塑性
NMDA受体
突触后电位
长时程增强
兴奋性突触后电位
细胞生物学
谷氨酸受体
遗传学
作者
Yuko Fukata,Hillel Adesnik,Tsuyoshi Iwanaga,David S. Bredt,Roger A. Nicoll,Masaki Fukata
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2006-09-22
卷期号:313 (5794): 1792-1795
被引量:319
标识
DOI:10.1126/science.1129947
摘要
Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.
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