Researchers in the US have identified what may be the first known common denominator between different forms of epilepsy.
Carnegie Mellon University neuroscientists say that this denominator underlying inherited and sporadic epilepsy the underlying may be a disruption in an ion channel called the BK channel, previously linked with familial epilepsy.
The BK channel allows electrically charged potassium ions into and out of cells. This activity starts and stops the electrical impulses by which neurons communicate with one another.
Barth and her colleagues carried out in vitro studies to investigate BK channels' function following a first seizure.
They found that after a seizure, BK channels become abnormally active function - neurons fired quicker, stronger and more spontaneously.
This abnormal activity might underlie the transition between a single seizure and the emergence of epilepsy, characterized by recurrent seizures.
"We've shown that BK antagonists can be very effective in normalizing aberrant electrical activity in neurons, which suggests that BK channel antagonists might be a new weapon in the arsenal against epilepsy," said Alison Barth, an assistant professor of biological sciences at Carnegie Mellon's Mellon College of Science.
"We found that seizures caused cells to become more excitable, and that BK channel antagonists bring everything back to normal. These channels are at a nexus of control and represent a new target for anticonvulsant therapies.
"The fact that the BK channel previously has been linked with familial epilepsy and with generalized seizures in subjects without a genetic predisposition points to a common therapeutic pathway.
"Although research has revealed that many types of inherited epilepsy are linked to mutations in different ion channels, there has been little overlap between these ion channels and those channels that are affected by sporadic or acquired forms of epilepsy. BK channels could represent a common pathway activated in familial and sporadic cases of epilepsy."
The findings are published in the June issue of Neurobiology of Disease.