Ketamine is a new type of medication that works differently than those used previously. It triggers reactions in the brain that enable brain connections to regrow, making it unique as an antidepressant.
Research into ketamine as an antidepressant began in the 1990s when it was discovered that certain drugs given to treat other diseases like high blood pressure and tuberculosis drastically affected people’s moods.
Research showed that serotonin and SSRIs didn’t fully explain depression, and that GABA and glutamate were responsible for regulating the majority of brain activity, including mood. Stress can also affect glutamate signaling, making neurons less adaptable and less able to communicate with other neurons.
Ketamine, a drug used as anesthesia during surgeries, triggers glutamate production, which prompts the brain to form new neural connections, making the brain more adaptable.
Further neuroscience research suggested that there was an abnormality within the glutamatergic system in the brains of people suffering from depression.
Researchers at Yale have been using subanesthetic doses of ketamine delivered intravenously in controlled clinic settings for patients with severe depression who have not improved with standard antidepressant treatments.
Ketamine may be effective as part of a comprehensive treatment plan for depression, but it is unlikely to cure depression on its own. Instead, it may help patients develop new neural pathways that can help them develop resiliency and protect against the return of the depression.
The FDA-approved drug esketamine works similarly to ketamine, but is two to five times more potent and can be taken in an outpatient treatment setting.
Ketamine comes with its cautions, including dizziness, a rise in blood pressure, and feelings of detachment or disconnection from reality.
Esketamine is not considered a first-line treatment option for depression, and is only prescribed for people who have tried two other depression medications without success.