Looking into the science and history of Ketamine: Ketamine was first used clinically in the 1960’s as an anesthetic. It was originally derived as an analog from phencycline in 1962 by Park Davis consultant and an organic chemist, Calvin Stevins. Since then, it has become widely used today as a powerful and common drug to provide patients with anesthesia and pain treatments. It is known to produce an unusual state in high doses and has become known as a “dissociative anesthetic.” This state causes patients to almost appear awake, keeping important reflexes intact such as airway and respiratory drive but without feeling pain or aware of other sensory inputs. Because of this, it has become a widely used anesthetic agent with an excellent safety profile that has been studied extensively. Interestingly, researchers began to see that lower doses of ketamine were incidentally helping patients with depression. By the 1990’s, researchers at Yale began to use very small doses of ketamine in patients with depression that weren’t improving with standard therapy and the results were incredible.
Ketamine works at the very level of our brain’s communication system by triggering certain molecules that have been found to have a major impact on neuroplasticity, which is how the brain can form new connections and communication over the course of a lifetime.
There are billions of neurons that make up our brain. These neurons are rapidly making connections and communicating with each other billions of times a day. The way that one neuron communicates with another neuron is by sending a molecule known as a neurotransmitter across a very small gap called the synaptic cleft. These tiny neurotransmitters get released from one neuron, travel across the synaptic cleft, and then bind to a receptor on the other neuron. This binding mechanism allows the next neuron to produce another signal down its cell membrane to the next neuron, and so on and so on.
Ketamine works by increasing a neurotransmitter called glutamate. Glutamate plays a major role in neuroplasticity by helping to form new connections between neurons. When the brain is under high stress for long periods of time, our neurons can shrink over time allowing less response to other neurons. Patients to suffer from common mental health disorders like depression and anxiety seem to suffer from this phenomena and lower glutamate levels. When glutamate levels surge in response to repeated ketamine treatments, the neurons appear to restore their communication and overall improves the brain’s neuroplasticity.
When Ketamine was first discovered and used in the 1960’s, it was known to the scientists that it worked by triggering glutamate. It wasn’t until later in the 1990’s, researchers began making the connection between levels of neurotransmitters, including glutamate, and depressive symptoms. Early research at Yale began to experiment with these hypotheses eventually leading to reveal small doses of ketamine in patients with mood disorders with incredibly positive results. Since then, myriad studies have been published and continuing research ongoing today regarding ketamine’s link to improving mood disorders.
It appears also that ketamine plays a role on opiate receptors and appears to have a role in neuronal pain. At low doses, ketamine inhibits a receptor on neurons called NMDA, which plays a role in amplifying pain signals. If ketamine inhibits this receptor, then pain signals should decrease in the brain. Ketamine also reacts with certain opioid receptors and may also have anti-inflammatory properties in order to produce pain relieving effects.
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