@article {10.3844/ajisp.2008.43.50,
article_type = {journal},
title = {Voltage-Gated Channels as Causative Agents for Epilepsies},
author = {Abuhamed, Mutasem and Bo, Xiao and Xia, Kun and Fang, Yi and Long, LiLi},
volume = {4},
year = {2008},
month = {Dec},
pages = {43-50},
doi = {10.3844/ajisp.2008.43.50},
url = {https://thescipub.com/abstract/ajisp.2008.43.50},
abstract = {Problem statement: Epilepsy is a common neurological disorder 
that afflicts 1-2% of the general population worldwide. It encompasses a variety 
of disorders with seizures. Approach: Idiopathic epilepsies were 
defined as a heterogeneous group of seizure disorders that show no underlying 
cause .Voltage-gated ion channels defect were recognized etiology of epilepsy 
in the central nervous system. The aim of this article was to provide an update 
on voltage-gated channels and their mutation as causative agents for epilepsies. 
We described the structures of the voltage-gated channels, discuss their current 
genetic studies, and then review the effects of voltage-gated channels as causative 
agents for epilepsies. Results: Channels control the flow of 
ions in and out of the cell causing depolarization and hyper polarization of the 
cell. Voltage-gated channels were classified into four types: Sodium, potassium 
calcium ands chloride. Voltage-gated channels were macromolecular protein complexes 
within the lipid membrane. They were divided into subunits. Each subunit had a 
specific function and was encoded by more than one gen. Conclusion: 
Current genetic studies of idiopathic epilepsies show the importance of genetic 
influence on Voltage-gated channels. Different genes may regulate a function in 
a channel; the channel defect was directly responsible for neuronal hyper excitability 
and seizures.},
journal = {American Journal of Immunology},
publisher = {Science Publications}
}