Acquired dendritic channelopathy in temporal lobe epilepsy
Acquired dendritic channelopathy in temporal lobe epilepsy
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DOI：
10.1126/science.1097065
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发表时间：
2004-07-23
期刊：
影响因子：
56.9
通讯作者：
Johnston, D
中科院分区：
文献类型：
--
作者：
Bernard, C;Anderson, A;Johnston, D
遗传性通道病是许多神经系统疾病的起源。在这里，我们报告了一种形式的通道病，是收购实验性颞叶癫痫（TLE），最常见的形式的癫痫在成年人。CA 1锥体神经元树突的兴奋性增加TLE，因为A型钾离子通道的可用性下降，由于转录（通道的损失）和翻译后（增加通道磷酸化细胞外信号调节激酶）机制。激酶抑制部分逆转树突的兴奋性控制水平。这种获得性通道病可能会放大神经元活动，并可能有助于TLE癫痫发作的启动和/或传播。
Inherited 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.