Ketamine is an anesthetic drug that works in the brain. It creates a “dissociative” state of mind.
It has a fast effect in the symptoms of depression that outlast the treatment session because it works with many different receptors in the brain. (Brain receptors are where the
medication connects to cause an effect.) A study in Yale university, found that one of the effects of Ketamine is an increase in “glutamate” production, which in a cascade of events, prompts the brain to form new neural connections. This is know as “Neuroplasticity”. When “Neuroplasticity” happens, the brain becomes more adaptable and able to create new pathways, giving a person the opportunity to develop more positive thoughts and behaviors.
Several receptors and neurotransmitters in the brain are involved in Mood control. N-
methyl-D-aspartate (NMDA) has a significant role in the etiology of depression. Ketamine is an
antagonist of these receptors, working very fast controlling symptoms of depression and acute
suicidal ideation.“Ketamine effects in chronic pain and as an antidepressant far outlast the actual drug levels and are probably mediated by a secondary increase in structural synaptic connectivity that is mediated by a neural response to the Ketamine-induced hyper-glutamatergic state. (sleigh 2014)”
Research
Ketamine which was widely used as anesthesia during surgeries, triggers glutamate production, which, in a complex, cascading series of events, prompts the brain to form new neural connections. This makes the brain more adaptable and able to create new pathways, and gives patients the opportunity to develop more positive thoughts and behaviors. This was an effect that had not been seen before, even with traditional antidepressants.
effects in chronic pain, and as an antidepressant, far outlast the actual drug levels and are probably mediated by a secondary increase in structural synaptic connectivity that is mediated by a neuronal response to the ketamine induced hyper-glutamatergic state.” (Sleigh 2014).
The N-methyl-D-aspartate (NMDA) receptor has a significant role in the etiology of depression. Ketamine, through its NMDA antagonistic action, works rapidly in controlling symptoms of depression and acute suicidal ideation. Ketamine may increase glutamate levels and lead to
synaptogenesis and elevated levels of brain-derived neurotrophic factor (BDNF). Severe depressive disorder is among most debilitating condition. Conventional pharmacotherapy usually takes several weeks (usually 4–12 weeks) to improve symptoms. Ketamine is an N methyl-D aspartate receptor antagonist having rapid action on depressive symptoms.
One popular theory was the serotonin hypothesis, which asserted that people with depression had low levels of a neurotransmitter called serotonin. This hypothesis came about by accident— certain drugs given to treat other diseases like high blood pressure and tuberculosis seemed to drastically affect people’s moods. Those that lowered serotonin levels caused depression- like symptoms; others that raised serotonin levels created euphoric-like feelings in depressed patients. This discovery ushered in a new class of drugs meant to treat depression, known as selective serotonin reuptake inhibitors (SSRIs). The first one developed for the mass market was Prozac. But eventually it became clear that the serotonin hypothesis didn’t fully explain depression. Not only were SSRIs of limited help to more than one-third of the people given them for depression, but growing research showed that the neurotransmitters these drugs target (like serotonin) account for less than 20 percent of the neurotransmitters in a person’s brain. The other 80 percent are neurotransmitters called GABA and glutamate. GABA and glutamate were known to play a role in seizure disorders and schizophrenia. Together, the two neurotransmitters form a complex push-and-pull response, sparking and stopping electrical activity in the brain. Researchers believe they may be responsible for regulating the majority of brain activity, including mood.
Intense stress can alter glutamate signaling in the brain and have effects on the neurons that make them less adaptable and less able to communicate with other neurons. This means stress and depression themselves make it harder to deal with negative events, a cycle that can make matters even worse for people struggling with difficult life events. Ketamine—from anesthetic to depression “miracle drug”
