MOLECULAR PLASTICITY
Dendritic ion channelopathy in acquired epilepsy
Article first published online: 7 DEC 2012
DOI: 10.1111/epi.12033
Wiley Periodicals, Inc. © 2012 International League Against Epilepsy
Issue

Epilepsia
Special Issue: Modulation of Epileptogenicity: A Focus on Molecular Plasticity
Volume 53, Issue Supplement s9, pages 32–40, December 2012
Additional Information
How to Cite
Poolos, N. P. and Johnston, D. (2012), Dendritic ion channelopathy in acquired epilepsy. Epilepsia, 53: 32–40. doi: 10.1111/epi.12033
Publication History
- Issue published online: 7 DEC 2012
- Article first published online: 7 DEC 2012
- Abstract
- Article
- References
- Cited By
Keywords:
- Dendrites;
- Channelopathy;
- K+ channels;
- Na+ channels;
- Ca2+ channels;
- Hyperpolarization-activated, cyclic nucleotide-gated channels;
- Pyramidal neurons
Summary
Ion channel dysfunction or “channelopathy” is a proven cause of epilepsy in the relatively uncommon genetic epilepsies with Mendelian inheritance. But numerous examples of acquired channelopathy in experimental animal models of epilepsy following brain injury have also been demonstrated. Our understanding of channelopathy has grown due to advances in electrophysiology techniques that have allowed the study of ion channels in the dendrites of pyramidal neurons in cortex and hippocampus. The apical dendrites of pyramidal neurons comprise the vast majority of neuronal surface membrane area, and thus the majority of the neuronal ion channel population. Investigation of dendritic ion channels has demonstrated remarkable plasticity in ion channel localization and biophysical properties in epilepsy, many of which produce hyperexcitability and may contribute to the development and maintenance of the epileptic state. Herein we review recent advances in dendritic physiology and cell biology, and their relevance to epilepsy.

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