Acquired dendritic channelopathy in temporal lobe epilepsy

被引：349

作者：

Bernard, C ^{[1
]}

Anderson, A

Becker, A

Poolos, NP

Beck, H

Johnston, D

机构：

[1] Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA

[2] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA

[3] Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA

[4] INSERM, U29, F-13273 Marseille 09, France

[5] Univ Bonn, Med Ctr, Dept Neuropathol, D-53105 Bonn, Germany

[6] Univ Bonn, Med Ctr, Dept Epileptol, Lab Expt Epileptol, D-53105 Bonn, Germany

[7] Univ Washington, Dept Neurol, Seattle, WA 98104 USA

[8] Univ Washington, Reg Epilepsy Ctr, Seattle, WA 98104 USA

来源：

SCIENCE | 2004年 / 305卷 / 5683期

关键词：

D O I：

10.1126/science.1097065

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：532 / 535

页数：4

共 28 条

[1] The A-type potassium channel Kv4.2 is a substrate for the mitogen-activated protein kinase ERK [J].