Conclusion
depression, depressed
In the past two decades, ketamine has emerged as one of the most promising pharmacological treatments for depression since selective serotonin re-uptake inhibitors (SSRIs) became available. While the exact mechanism is unknown, it has been hypothesized that ketamine’s antidepressant effects are at least in part mediated by increases in neuroplasticity broadly, and by synaptogenic actions specifically. We found that a proxy for structural neuroplasticity was associated with treatment response to ketamine in a subset of the depression-relevant brain regions we examined. These results have important implications for the development of synergistic therapies and for understanding the neurobiological mechanisms by which ketamine exerts rapid antidepressant actions in depressed patients.