The anesthetic ketamine has spurred excitement in psychiatry for almost 20 years since researchers first showed that it alleviated depression in a matter of hours. The rapid reversal of symptoms contrasted sharply with the existing set of antidepressants, which take weeks to begin working. Subsequent studies have shown ketamine works for patients who have failed to respond to multiple other treatments and so are deemed “treatment-resistant.”
Despite this excitement, researchers still don’t know exactly how ketamine exerts its effects. A leading theory proposes that it stimulates regrowth of synapses (connections between neurons), effectively rewiring the brain.
Another reason ketamine has researchers excited is that it works differently than existing antidepressants. Rather than affecting one of the “monoamine” neurotransmitters (serotonin, norepinephrine, and dopamine), as standard antidepressants do, it acts on glutamate, the most common chemical messenger in the brain. Glutamate plays an important role in the changes synapses undergo in response to experiences that underlie learning and memory. That is why researchers suspected such neuroplasticity would lie at the heart of ketamine’s antidepressant effects.
Ketamine intravenous infusion therapy, which exhibits a 60%-70% success rate in clinical trials, has been shown to offer almost immediate relief (with minimal, if any, side effects) to those who suffer from severe mood disorders. For those patients who respond well to Ketamine, improvement is usually seen within one to two hours of receiving their first infusion, rather than weeks, or even months, as is the case with most traditional antidepressant medications.
