RIVERSIDE, Calif. Researchers at the University of California, Riverside have made a discovery in the lab that could help drug manufacturers develop new antiepileptic drugs and explore novel strategies for treating seizures associated with epilepsy a disease affecting about two million Americans.
Neurons, the basic building blocks of the nervous system, are cells that transmit information by electrical and chemical signaling. During epileptic seizures, which generally last from a few seconds to minutes and terminate spontaneously, the concentrations of ions both inside the neuron and the space outside the neuron change due to abnormal ion flow to and from neurons through ion "channels" tiny gateways that are embedded to the surface of the neuron.
Ordinarily, intracellular (inside the cell) sodium concentration is low compared to extracellular sodium (the reverse is true of potassium). During seizure, however, there is a buildup of intracellular sodium, with sodium ions moving into neurons from the extracellular space, and potassium ions doing the opposite.
To understand exactly how neurons function during epileptic seizures, Maxim Bazhenov, an associate professor of cell biology and neuroscience, and Giri P. Krishnan, a postdoctoral researcher in his lab, developed and used realistic computer simulations in their analyses and found that while there is a progressive and slow increase in intracellular sodium during seizure, it is this accumulation of intracellular sodium that leads to the termination of the seizure.
"According to our model, sodium concentration reaches a maximum just before the seizure terminates," Bazhenov said. "After seizure initiation, this intracellular sodium buildup is req
|Contact: Iqbal Pittalwala|
University of California - Riverside