It’s the first study to show in a multicellular system that the BPNT-1 protein might be the target for lithium’s action,” says York, who was not involved in the research. “This is an important step in showing a neural function for BPNT-1. John York, a professor of biochemistry at Vanderbilt University School of Medicine, says the findings are intriguing. They also found the same behavioral effects in worms treated with lithium. When the researchers knocked out the gene for BPNT1, they found that the ASJ neurons entered a dormant state and the worms could no longer execute either avoidance behavior or the dauer exit. To their surprise, one of the genes implicated by this screen was one that codes for a protein called BPNT1, which was already known to be inhibited by lithium.īPNT1 is a protein that removes phosphate groups from a compound known as PAP, a process that is critical to maintaining normal cell function. This reactivation, known as the dauer exit, occurs when food becomes more plentiful.Īs a follow-up to that study, the researchers performed a genetic screen in which they looked for mutated genes that disrupt ASJ neurons. Previous studies from other labs had shown that the ASJ neurons are also required for reawakening from a starvation-induced hibernation state. In a paper published in 2014, Meisel and Kim discovered that a pair of neurons known as ASJ neurons are necessary for the worm’s avoidance of harmful bacteria. This worm has a simple nervous system consisting of 302 neurons, most of which occur in pairs. The MIT team did not set out to study lithium but fell upon it while exploring interactions between Caenorhabditis elegans and its microbial environment. However, no studies have conclusively linked these targets to lithium’s effects on bipolar patients. Some of the hypothesized targets are an enzyme that produces inositol, a simple sugar involved in cell signaling, and an enzyme called GSK3, which inactivates other proteins. Lithium interacts with many proteins and other molecules in the brain, so it has been difficult for scientists to determine which of these interactions produce mood stabilization. Lithium’s ability to act as a tranquilizer for people suffering from mania and bipolar disorder was discovered in 1949 by the Australian psychiatrist John Cade, but the drug was not approved by the U.S. “There are hypotheses, but nothing’s been proven.”ĭennis Kim, an associate professor of biology, is the senior author of the paper, which appears in the July 7 issue of Current Biology. “How lithium acts on the brain has been this great mystery of psychopharmacology,” says Joshua Meisel, an MIT postdoc and lead author of the study. While these behavioral effects in worms can’t be translated directly to humans, the results suggest a possible mechanism for lithium’s effects on the brain, which the researchers believe is worth exploring further. In a study of worms, the researchers identified a key protein that is inhibited by lithium, making the worms less active. MIT biologists have now discovered a possible explanation for how lithium works. While the drug has a good success rate, scientists are still unsure exactly how it achieves its beneficial effects. doctors have prescribed lithium to treat patients with bipolar disorder.
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