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Science 23 July 2004:
Vol. 305. no. 5683, pp. 532 - 535
DOI: 10.1126/science.1097065
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Reports

Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy

Christophe Bernard,1,3* Anne Anderson,1,2 Albert Becker,4 Nicholas P. Poolos,1,6 Heinz Beck,5 Daniel Johnston1

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.

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.
6 Department of Neurology and Regional Epilepsy Center, University of Washington, Box 359745, 325 9th Avenue, Seattle, WA 98104, USA.

* To whom correspondence should be addressed. E-mail: cbernard{at}inmed.univ-mrs.fr

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