منابع مشابه
Ion channels and epilepsy
Ion channels play a central role in the generation and control of neuronal excitability. Genetic defects in ion channels are associated with several forms of human idiopathic epilepsies. These defects range from nonsense and missense point mutations to insertion, truncation and splice site mutations producing altered, non-functional or negative-dominant channel subunits. To date, 12 mutated gen...
متن کاملIon channels and epilepsy.
Ion channels provide the basis for the regulation of excitability in the central nervous system and in other excitable tissues such as skeletal and heart muscle. Consequently, mutations in ion channel encoding genes are found in a variety of inherited diseases associated with hyper- or hypoexcitability of the affected tissue, the so-called 'channelopathies.' An increasing number of epileptic sy...
متن کاملIon channels in epilepsy.
Neuronal excitability is determined by the flux of ions through ion channels. Many types of ion channels are expressed in the central nervous system, each responsible for its own aspect of neuronal excitability, from postsynaptic depolarization to action potential generation to neurotransmitter release. These mechanisms are tightly regulated to create a balance between excitation and inhibition...
متن کاملReview Ion channels and epilepsy
In order for cells to retain their integrity to water and yet permeate charged ions, the phospholipid cell membrane contains transmembrane proteins that allow the passage of specific ions from the interior of the cell to outside, and vice versa. There is a huge diversity of these ion channels. Some are tissuespecific; others are widely distributed throughout the body. They contribute to the mai...
متن کاملEpilepsy and other neurological disorders Ion channels and epilepsy
Ion channels play a central role in the generation and control of neuronal excitability. Genetic defects in ion channels are associated with several forms of human idiopathic epilepsies. These defects range from nonsense and missense point mutations to insertion, truncation and splice site mutations producing altered, non-functional or negative-dominant channel subunits. To date, 12 mutated gen...
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ژورنال
عنوان ژورنال: QJM
سال: 2006
ISSN: 1460-2725,1460-2393
DOI: 10.1093/qjmed/hcl021