Anti-epileptic drug (AED) therapy is effective in two-thirds of individuals with epilepsy, but they are not beneficial in the remaining patients. These patients are called “refractory,” and treatment options for them include neurostimulation, dietary therapies and brain surgery.
One neurostimulation technique used in refractory epilepsy is called deep brain stimulation (DBS), a technique where electrodes are implanted and electrical impulses are delivered to specific parts of the brain. For epilepsy, DBS has been effective when a part of the brain called the anterior thalamic nucleus was stimulated. However, the reason why DBS is effective in epilepsy is not fully understood. Recently, scientists published a study in an effort to understand how DBS works. If we understand the mechanism of action underlying DBS, we can hopefully find ways to make DBS more effective for people with refractory epilepsy.
The scientists wanted to examine whether a compound called adenosine was responsible for efficacy of DBS. Adenosine has been shown to decrease seizures in the lab in animal models, allowing the scientists to hypothesize that DBS decreases seizure frequency by releasing adenosine.
Epilepsy in the lab can be simulated in experimental animals by injecting them with drugs called chemoconvulsants. One of these drugs is pilocarpine. In this study, the scientists administered pilocarpine to rats and addressed the hypothesis in two parts:
By using a variety of experimental tools in experimental rats, the scientists found:
by Sloka Iyengar, PhD
Basic Science Editor