Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy-Reference-Cited by-同舟云学术

Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy

Published:2004-07-23 Issue:5683 Volume:305 Page:532-535
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Bernard Christophe¹²³⁴⁵,Anderson Anne¹²³⁴⁵,Becker Albert¹²³⁴⁵,Poolos Nicholas P.¹²³⁴⁵,Beck Heinz¹²³⁴⁵,Johnston Daniel¹²³⁴⁵

Affiliation:

1. Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.

2. Department of Pediatrics and Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.

3. INSERM U29, 163 Route de Luminy BP13, 13273 Marseille Cédex 09, France.

4. Department of Neuropathology, Laboratory of Experimental Epileptology, University of Bonn Medical Center, Sigmund-Freud Strasse 25, 53105 Bonn, Germany.

5. Department of Epileptology, Laboratory of Experimental Epileptology, University of Bonn Medical Center, Sigmund-Freud Strasse 25, 53105 Bonn, Germany.

Abstract

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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