![]() Overall, Sato and Woolley show that the production of estrogen in the brain escalates seizure activity, and suggest that aromatase inhibitors may be useful for controlling seizures. The drug strongly suppressed seizures, whereas control rats that did not receive the injection continued to have seizures. Sato and Woolley tested this by injecting rats with a drug that inhibits estrogen production, called an aromatase inhibitor, shortly after seizures began. Because estrogens are known to increase the activity of cells in the hippocampus, this suggested that estrogens that are produced in the brain during seizures could make seizures worse. Sato and Woolley studied male and female rats and found that in both sexes, seizures stimulate the production of estrogens in the hippocampus – a part of the brain that is often involved in seizures. Sato and Woolley therefore set out to test a two-part hypothesis: that seizures stimulate the production of estrogen in the brain, and that inhibiting this production process just as seizures begin would make seizures less severe. However, estrogens are also made in the brain of both sexes, where they could promote activity during seizures. Most people think of estrogens as being female sex hormones. A better alternative would be to target a factor that promotes activity especially during seizures. Although this is often effective in controlling seizures, it can also lead to negative side effects like drowsiness, dizziness or difficulty concentrating. Current anti-seizure medications work by reducing brain activity generally. ![]() Seizures occur when connected groups of cells in the brain become over-active and fire together. These results reveal neurosteroid estrogen synthesis as a previously unknown factor in the escalation of seizures and suggest that acute administration of aromatase inhibitors may be an effective treatment for SE. Consistent with a seizure-promoting effect of hippocampal estrogen synthesis, intra-hippocampal aromatase inhibition also suppressed seizures. Hippocampal E2 levels were higher in rats experiencing more severe seizures. We found that KA-induced SE stimulates synthesis of estradiol (E2) in the hippocampus, a brain region commonly involved in seizures and where E2 is known to acutely promote neural activity. Here, we show in rats that systemic administration of an aromatase (estrogen synthase) inhibitor after seizure onset strongly suppresses both electrographic and behavioral seizures induced by kainic acid (KA). In vitro studies suggest a novel approach to controlling seizures in SE: acute inhibition of estrogen synthesis in the brain. Status epilepticus (SE) is a common neurological emergency for which new treatments are needed.
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