生物谷報道：最新一項研究表明,，大腦的A型鉀通道直接與顳葉癲癇相關(guān)，它是最常見的一種癲癇類型,。這種通道的轉(zhuǎn)錄水平改變,，或轉(zhuǎn)錄后的翻譯水平改變,，導(dǎo)致通道的數(shù)量變化，從而直接影響了海馬CA1區(qū)細(xì)胞的激活方式,，從而成為了癲癇誘發(fā)的真正原因,。在遺傳性癲癇中也有類似情況，這一研究從細(xì)胞離子通道角度揭示了癲癇的電生理學(xué)原理,。這篇文章發(fā)表在剛剛出版的Science上.
channelopathies are at the origin of many neurological disorders. Here we report a form of channelopathy that is acquired in experimental temporal lobe epilepsy (TLE), the most common form of epilepsy in adults. The excitability of CA1 pyramidal neuron dendrites was increased in TLE because of decreased availability of A-type potassium ion channels due to transcriptional (loss of channels) and posttranslational (increased channel phosphorylation by extracellular signal-regulated kinase) mechanisms. Kinase inhibition partly reversed dendritic excitability to control levels. Such acquired channelopathy is likely to amplify neuronal activity and may contribute to the initiation and/or propagation of seizures in TLE.
