Dendritic h Channelopathy in Epileptogenesis
نویسندگان
چکیده
منابع مشابه
Dendritic h Channelopathy in Epileptogenesis
Recent work has suggested a link between h channels and epilepsy. In this issue of Neuron, Shah et al. demonstrate that a robust, postseizure decrease in h channels during a critical phase of epileptogenesis mechanistically underlies dendritic hyperexcitability in entorhinal-hippocampal pyramidal cells.
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Ion channelopathy plays an important role in human epilepsy with a genetic cause and has been hypothesized to occur in epilepsy after acquired insults to the CNS as well. Acquired alterations of ion channel function occur after induction of status epilepticus (SE) in animal models of epilepsy, but it is unclear how they correlate with the onset of spontaneous seizures. We examined the propertie...
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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 allow...
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http://www.sciencemag.org/cgi/content/full/305/5683/532 version of this article at: including high-resolution figures, can be found in the online Updated information and services, http://www.sciencemag.org/cgi/content/full/305/5683/532/DC1 can be found at: Supporting Online Material found at: can be related to this article A list of selected additional articles on the Science Web sites http://w...
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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 chan...
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ژورنال
عنوان ژورنال: Neuron
سال: 2004
ISSN: 0896-6273
DOI: 10.1016/j.neuron.2004.10.018