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  • Writer's pictureLogan MacLean

A Brief Introduction to Ketamine Infusion Therapy

The medication known as ketamine has been around for approximately half a century. First synthesized in 1962 and approved by the FDA in 1970, ketamine has been commonly used in the operating room and on the battlefield for over 50 years. Ketamine is classified as a dissociative anesthetic since it can distort the perception of visual and auditory stimuli and acutely cause the patient to feel detached from the environment and oneself.

In the operating room, ketamine can be used as a general anesthetic induction agent (making the patient go to sleep) when injected over a short time frame at high doses. It is also commonly used to provide additional pain relief to patients and decrease the amount of narcotics given to patients undergoing more invasive surgery.

Over the past 20 years, numerous studies have examined ketamine’s effects within the field of mental health when given in low doses over a longer duration (about an hour). The results have been extremely promising regarding the speed of responses compared to traditional medications, as well as patients’ responses to ketamine. Currently, ketamine is being used to treat major depressive disorder, bipolar disorder, suicidality, generalized anxiety disorder, OCD, and PTSD.

The way ketamine affects the brain is complicated, and we are still learning about the different pathways ketamine influences that lead to its rapid effects. The key neurotransmitter that ketamine directly changes in different regions of the brain is called glutamate. This leads to both short-term and long-term effects.

Within a couple of hours of ketamine infusion, patients may be able to feel its antidepressant effects. This is due to ketamine’s effects on the release of glutamate in the prefrontal cortex, hippocampus, and amygdala. This leads to rapid antidepressant effects that occur within hours of treatment.

Long term, ketamine aids in the restoration of impaired neurons. Neurons are the signaling centers that allow messages to pass to and from, as well as within your brain. Neurons are composed of dendrites (receive signals from other cells), a cell body (regulates the function of the neuron), and an axon (sends signals out to other cells). Ketamine increases the density of the dendrites (increases dendritic spine number) through increasing brain-derived neurotrophic factor (BDNF). Simply put, ketamine increases the number of receptors that the neuron has lost, which allows for more efficient communication between neurons. These increases occur approximately 2-7 days after an infusion and are believed to be the cause of the longer-term antidepressant effects of ketamine.

Overall, ketamine rapidly facilitates improved inter-neuron communication in the prefrontal cortex and hippocampus, as well as reduces amygdala hyperreactivity to emotional stimuli. Additionally, because of ketamine’s effect on dendrite density (increasing the neuron’s ability to receive neurotransmitters), it works synergistically with other antidepressants since these antidepressants work to increase the amount of neurotransmitters in specific regions of the brain.

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