Researchers at the Baylor College of Medicine in Houston, Texas hypothesised that these therapies are unintendedly suppressing interneurons that would otherwise help to rein in harmful neural activity.
To test this, they used stargazer mice, which have a single mutated chromosome that causes symptoms characteristic of absence seizures – which are usually less than 20 seconds long and often go undiagnosed – in humans.
They administered CPP and MK-801 – two chemicals that are usually successful in treating absence epilepsy models by blocking NMDA receptors in the brain.
In the stargazer mice, however, the treatment routinely made seizures worse. Further analysis revealed that these subjects all shared a cortical interneuron defect, which meant that inhibitory neurons were not activated normally and relied entirely on the NMDA receptors to function.
“[The findings] define an interneuron-dependent mechanism for paradoxical seizure exacerbation in absence epilepsy,” the researchers concluded.
Originally Posted by Steve Long @ Epilepsy Research UK