New Pathway to Epilepsy Discovered

Rat study helps find previously unknown change in neurons

THURSDAY, July 22, 2004 (HealthDayNews) -- Working with rats, scientists have uncovered a previously unknown change in brain cells that appears to be responsible for the seizures associated with the most common type of adult epilepsy.

In rats with a condition resembling the condition, known as temporal lobe epilepsy, the ends of these neurons, called dendrites, were more sensitive than normal brain cells. Epilepsy causes neurons to die, and the resulting fewer-than-normal number of dendrites allows too much potassium to pass through the cell. This, in turn, caused increased sensitivity and seizures.

Targeting this potassium channel may open the way to new treatments for epilepsy, researchers report in the July 23 issue of Science.

Epilepsy is a brain disorder in which neurons fire abnormally. The normal pattern of brain activity becomes disturbed, causing strange sensations, emotions and behavior. It can also sometimes lead to convulsions, muscle spasms and loss of consciousness.

According to the Epilepsy Foundation, some 2.5 million Americans suffer from epilepsy and seizures.

"We have been exploring the properties of dendrites, which are the tree-like parts of neurons that receive connections from other neurons by way of synapses," said lead researcher Daniel Johnston, a professor of neuroscience at Baylor College of Medicine.

Dendrites have many ion channels, which are specialized proteins that allow ions to flow in and out of brain cells, Johnston explained. These ions control the electric activity of neurons.

Johnston's team found that, in epilepsy, the number of potassium ion channels was significantly reduced. "The channels that remained were altered," he added.

The net effect of fewer potassium channels and damaged channels made the cells more likely to fire in a hyperexcitable state. "That is the hallmark of epilepsy," Johnston said.

"Drugs that target this ion channel would be a totally novel way of potentially suppressing this hyperexcitable state," he added.

How potassium channels become altered is not known. It is possible that seizures themselves may damage the neurons, and once that begins, the damage continues until epilepsy develops, said co-researcher Dr. Nicholas P. Poolos, an assistant professor of neurology at the University of Washington.

In addition, in epilepsy that is inherited, which most temporal epilepsy isn't, the cause has been identified as mutations in genes that control ion channels, he added.

"Ion channels are really the basis of a number of epilepsy syndromes. And our studies in animals are getting us to think more about how ion channels are affected in humans when epilepsy is not inherited but acquired later in life," Poolos said.

"We would like to understand the period from the first seizure and development of chronic epilepsy, which leads to fewer potassium channels," Johnston said.

"This is another big clue to how the brain circuits are changing and why epileptics are predisposed to seizures," said Dr. Kevin J. Staley, a professor of pediatrics and neurology at the University of Colorado Health Sciences Center.

"These findings give a molecular target to dampen seizures and gives us an understanding of how neurons adapt to changing conditions," said Staley, who wrote an editorial accompanying the article. "These finding also help us understand how we recover from brain injury."

More information

The National Institute of Neurological Disorders and Stroke helps explain epilepsy.

Related Stories

No stories found.
logo
www.healthday.com