Research shows that seizure suppression was associated with an increase in COX-2 expression in neurons.
James Hewett, associate professor of biology, and Yifan Gong, a Ph.D. candidate in biology and neuroscience, have co-authored an article in the journal Neuroscience (Elsevier, 2018) about a protein in the brain called T-cell intracellular antigen-1 (TIA-1).
“TIA-1 is known for its ability to regulate gene expression during cellular stress,” says Hewett, who studies the processes that suppress the severe electrical storms in the brain, leading to seizures. “We suspected that TIA-1 was involved with seizure suppression, but our findings suggested something else.”
He and Gong are interested in the function of an enzyme in the brain called cyclooxygenase-2 (COX-2). This enzyme makes prostaglandins — chemical messengers that aid in the performance of normal tasks, including learning and memory.
“Our findings raise the possibility that the level of neuronal COX-2 expression in the brain may be a determinant of the seizure threshold [a natural set-point for electrical activity, above which seizures occur]. This suggests that a better understanding of the regulation of COX-2 expression in the brain can provide new insights into molecular mechanisms that suppress seizure-induction,” adds Hewett, a pharmacologist by training.