Ketamine has been available as an anesthetic for many years but started to be investigated as an antidepressant in early 2000. Ketamine works differently than traditional antidepressants including SSRI’s, though researchers are still trying to pinpoint the exact mechanism behind the efficacy. Because Ketamine exerts an antidepressant effect through a new and novel mechanism, it offers extensive success to help people successfully topple depression when other treatments have failed.
In low-doses, ketamine produces a surge in glutamate. Glutamate is an excitatory neurotransmitter that encourages the growth of brain synapses. With an increase in glutamate, the neural connections in the regions of the brain that are affected by depression become stimulated, strengthened, and restored very quickly. The brain circuitry and function is vastly improved from these strengthened neurons that have previously been stifled due to depression.
Researchers have also studied molecular changes with ketamine treatments that are related to G Proteins. People with depression typically have a high amount of G proteins that have accumulated but are inactive. SSRIs activate the G proteins into useful activity. Ketamine quickly jumpstarts and forces G proteins to be active much faster, as in minutes instead of weeks, and keeps G proteins in action for much longer. This process likely affects mood, thought patters and cognition.
Ketamine may also alleviate depression by other means. For example Ketamine might reduce inflammatory signals which has been linked to mood disorders. It might also help facilitate communication between cells in very specific brain areas. Most likely, ketamine works in a multitude of ways at the same time. A lot about Ketamine is still being investigated.