sodes when the brain did not have the proper theta rhythm.
The researchers also found that when the theta rhythm was induced in the rats, it reduced epileptic discharges 86-97%. (The researchers induced theta in one of three ways – by regulating the rats’ anesthesia, by stimulating the septum directly with an injection of carbachol, or by using the sensory stimulation method of pinching the tail.)
The amplitude and frequency of the theta rhythm of the epileptic rats was significantly altered compared to the control group. In effect, the theta rhythm became faster and more jittery. Also, the septal neurons of epileptic rats doubled their firing rates in relation to the controls, from about 14 spikes per second to about 29 spikes per second.
Two promising lines of research
Colom and his fellow researchers at the University of Texas at Brownsville/Texas Southmost College are looking at two different approaches to stopping epilepsy. One group is taking the approach of making the neurons less excitable (this effort is led by Emilio Garrido-Sanabria and Masoud Zarei). Colom’s group is looking for a new treatment that will focus on inducing theta.
“The understanding of the theta rhythm’s anti-epileptic effect at the cellular and molecular levels may result in novel therapeutic approaches dedicated to protect the brain against abnormal excitability states,” the authors wrote.
Although this research gives more insight into how epilepsy occurs, a cure is still years away. “But I would say there is hope,” Colom said. “We want to offer people with epilepsy new options,” he said, but progress will depend upon funding, he added.
The researchers will repeat the study using animals that are awake and mobile, though it is more difficult to record the brain’s discharges in freely moving animals. Then the research can move to humans.
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