Amygdala: The amygdala is an integral component of the limbic system. It is important in emotional processing, memory formation, and regulating fear, aggression, and stress responses.
BDNF (Brain-Derived Neurotrophic Factor): A protein found in the brain and spinal cord that supports the survival of existing neurons and encourages the growth and differentiation of new neurons and synapses. It is active at all nerve cell connections. BDNF also helps regulate synaptic plasticity. There is some evidence that Ketamine increases BDNF levels, which might play a role in its antidepressant effects.1
Dendrite: A dendrite is a branched, tree-like extension of a neuron that receives electrical and chemical signals from other neurons. The dendrites convey the received signals to the neuron’s cell body, or soma, where the signals are further processed. The structure and complexity of dendrites can vary greatly between different types of neurons and are important for the functioning of neural networks in the brain and nervous system. Ketamine is theorized to work by improving the density and function of dendrites.
Depression (unipolar depression): Depression, or Major Depressive Disorder, is characterized by persistent low mood and impaired daily functioning. Symptoms include two weeks or more of depressed mood or anhedonia (absence of feelings or pleasure) with problems with thinking and concentrating, sleep disturbances, appetite changes, suicidal thoughts, excessive feelings of guilt, impaired motivation, thoughts about death or suicide, low energy, weight changes, or feelings of worthlessness.
Double-blind: In a therapeutic study, neither the researcher nor the participant are aware of who is getting the actual treatment versus the placebo.
Glutamate: The primary excitatory neurotransmitter in the brain. Dysfunction in Glutamate is related to many psychiatric conditions, including mood disorders and anxiety. Ketamine’s action on the NMDA receptor and its influence on glutamate transmission is one of the ways it can result in rapid antidepressant effects.¹
Hippocampus: A region of the brain involved in memory formation, stress response, learning, and mood regulation. The hippocampus is part of the limbic system. Hippocampus changes are linked to mental health disorders such as depression, anxiety, and post-traumatic stress disorder.
Intravenous (IV) Infusion Therapy: Infusion therapy involves inserting a needle into the vein to place a small catheter, which can then deliver drugs directly into the bloodstream in a controlled manner over time. IV therapy is often a faster, more effective way to receive medication.
Ketamine: Ketamine is a dissociative anesthetic known for its ability to produce feelings of detachment from one’s environment and self. Ketamine was approved in 1970 by the FDA as an anesthetic used for anesthesia, sedation, and pain relief.¹ It’s known for being an effective and safe alternative to general anesthesia because it doesn’t generally slow heart rate or breathing, unlike other anesthetic drugs. 2 Ketamine works by blocking NMDA receptors in the brain. At high doses, it can have dissociative and hallucinogenic effects. It has been found to have rapid antidepressant effects, even at low doses. Ketamine is prescribed off-label to treat treatment-resistant depression, suicidality, and other psychiatric conditions.
Limbic System: The limbic system is a collection of brain structures that regulate emotions and memory. Abnormalities in the limbic system are associated with many psychiatric disorders.
Neurons: Neurons are specialized cells that constitute the nervous system, encompassing the brain, spinal cord, and peripheral nerves in the body. Designed to receive and convey information, they communicate using electrical and chemical signals. Each neuron consists of a central cell body, or soma, from which dendrites branch out to receive messages from other neurons. Extending from the soma is a long axon that relays signals to other neurons, muscles, or glands.¹
Neuroplasticity: Neuroplasticity or synaptic plasticity refers to the ability of the neural networks in the brain to adapt through growth and reorganization.¹ The strength or weakness of neural connections or synapses is important for development, learning new skills, memory formation, recovering from brain injuries, and adapting to change.¹ Ketamine promotes neuroplasticity, which might underlie some of its antidepressant effects and may be why many clients experience long-lasting benefits even after stopping ketamine therapy.¹
Neurotransmitters: Neurotransmitters are chemical messengers released from neurons to transmit signals to other neurons. The most common neurotransmitter is Glutamate, produced by most neurons in the brain. Glutamate plays a role in synaptic plasticity and cognitive functions such as learning and memory. Changes in Glutamate transmission are one of the primary mechanisms by which Ketamine works to alleviate depression and other illnesses.
N-Methyl D-Aspartate (NMDA) receptor: The NMDA receptor acts as a “docking site” on neurons for Ketamine to bind, affecting brain electrochemical pathways.¹ The NMDA receptor plays a role in cognition, chronic pain, synaptic plasticity, mood regulation, memory function, and the development of depression.3 Ketamine blocks this receptor, causing an increase in the excitatory neurotransmitter glutamate and other cellular processes that support healthy neurons and the formation of new synapses.
Off-label: Prescribing an FDA-approved drug for an unapproved indication, population, form, or dosage. Off-label is prevalent in medicine and occurs when there is evidence to support the therapeutic use of a drug, but there has yet to be formal approval by regulatory agencies. Approximately 20% of all drugs used in psychiatry are prescribed off-label. Evidence supporting off-label use comprises expert consensus, clinical studies, and case reports. Use requires careful evaluation by a medical provider of the risks and benefits of a drug.4
Open-Label: In an open-label study, the researcher and the participants know the treatment being given, meaning there is no blinding of the tested treatment. This is opposite to a double-blind study, where neither the participants nor the researchers know which treatment is being given.
Placebo: In research studies, effects can emerge from the researchers’ and participants’ expectations regarding the treatment. By using a placebo control — an inert treatment with no therapeutic effect — researchers can differentiate between the actual impact of the treatment and the influence of these expectations on the results.
Post-Traumatic Stress Disorder (PTSD): PTSD is a mental health condition that can develop after an individual has experienced or witnessed a traumatic event. Symptoms include re-living the traumatic event through intrusive thoughts or flashbacks, avoidance behaviors, persistent negative alterations in cognition and mood, and hyperreactivity to stimuli.
Prefrontal Cortex: This is the brain region responsible for executive functioning or higher-level thinking. It also plays a role in personality expression and emotional regulation. Abnormalities in the prefrontal cortex have been linked to mental health disorders such as depression, attention-deficit hyperactivity disorder, and anxiety.
Psychedelic experience: Consuming a psychedelic substance can induce a psychedelic state, or “trip,” characterized by altered perception, thinking, and feeling. A person in a psychedelic state may experience an altered state of consciousness. Individuals can have sensory alterations, hallucinations, altered time perception, ego dissolution, emotional amplification, sense of unity, spiritual experiences, or enhanced insight.5 The nature and intensity of a psychedelic experience can vary widely based on several factors, including the specific substance, dosage, individual’s mindset, and the setting in which the substance is taken.
Psychomimetic effects: Refers to the dissociative effects caused by Ketamine, typically at higher or more rapid doses, such as depersonalization (a person feeling unreal), derealization (the world looking strange), and hallucinations.
Randomized: Participants are assigned to receive either the actual or placebo treatment by chance.
Rapid-Acting Antidepressant Drug (RAAD): Ketamine has been designated within a new class of drugs classified as RAADs due to substantial evidence demonstrating ketamine’s unique ability to rapidly have antidepressant effects, often over hours or days. Standard treatments such as antidepressant medications can take several weeks to begin working and up to six weeks for full effect.6
Remission: A strong response to treatment with a marked decrease in intensity and number of symptoms, often given as a cut-off point on rating scales where the individual no longer meets the criteria for a mental health disorder.¹Individuals can be in partial remission, where they may continue to experience some symptoms, or full remission, where the individual is asymptomatic.⁴
Response: In a therapeutic study, a response is defined as a 50% reduction in symptom severity relative to its level before the study.
Synapse: The junctions where neurons communicate with other cells are called synapses. Electrical impulses travel along the axon, releasing neurotransmitters at the synapse, which then bind to receptors on the neighboring cell, facilitating the transfer of information. Neurons can also communicate through direct electrical connections.
Treatment-Resistant Depression (TRD): Refers to major depressive disorder where at least two different trials of antidepressant treatments for the current depressive episode have failed to have a response.⁵
If you or your loved one are suffering with depression, ketamine therapy may be a great next step for you. Feel free to call Kure Medical or your local ketamine center to learn more about ketamine infusion therapy. If this is an emergency please call the National Mental Health Hotline: 988 or call the National Emergency Hotline: 911
Disclaimer: This blog is for informational purposes only and does not constitute medical advice. Please consult with a healthcare professional for personalized recommendations and guidance regarding ketamine therapy.
- Hyde, S. J. (2015). Ketamine for depression. Xlibris. ↩︎
- Cohen, S. P., Bhatia, A., Buvanendran, A., Schwenk, E. S., Wasan, A. D., Hurley, R. W., Viscusi, E. R., Narouze, S., Davis, F. N., Ritchie, E. C., Lubenow, T. R., & Hooten, W. M. (2018). Consensus Guidelines on the Use of Intravenous Ketamine Infusions for Chronic Pain From the American Society of Regional Anesthesia and Pain Medicine, the American Academy of Pain Medicine, and the American Society of Anesthesiologists. Regional anesthesia and pain medicine, 43(5), 521–546. https://doi.org/10.1097/AAP.0000000000000808 ↩︎
- Kennedy S. (2002). Full remission: a return to normal functioning. Journal of psychiatry & neuroscience : JPN, 27(4), 233–234. ↩︎
- U.S. Food and Drug Administration. (2018, February 5). Understanding unapproved use of approved drugs “Off label.” https://www.fda.gov/patients/learn-about-expanded-access-and-other-treatment-options/understanding-unapproved-use-approved-drugs-label
↩︎ - Grob, C. S., & Grigsby, J. (2022). Handbook of Medical hallucinogens. The Guilford Press. ↩︎
- Abdallah, C. G., & Krystal, J. H. (2020). Ketamine and rapid acting antidepressants: Are we ready to cure, rather than treat depression?. Behavioural brain research, 390, 112628. https://doi.org/10.1016/j.bbr.2020.112628 ↩︎
