When used to treat depression and anxiety, ketamine has a different mechanism of action from standard antidepressants. Ketamine acts by blocking N–methyl–d–aspartate (NMDA) receptors in the brain, which interact with the neurotransmitter glutamate. A 2018 article in the journal Nature concluded that depression is associated with increased burst activity in a part of the brain called the lateral habenula, which is essentially the “anti-reward center.” As a rapid antidepressant, ketamine works by blocking NMDA receptors in the lateral habenula. The resulting chemical changes in the brain are not yet fully understood, but likely involve ketamine-induced gene expression and signaling cascades that continue to act long after the drug has been eliminated from the body.