How Ketamine Therapy Works

The science behind one of psychiatry's most significant breakthroughs. Understanding how ketamine creates rapid, lasting change in the brain.

1962
First Synthesized
NMDA
Primary Target
Glutamate
Key Neurotransmitter
BDNF
Growth Factor

A Different Kind of Antidepressant

Most antidepressants work by increasing serotonin, norepinephrine, or dopamine in the brain. Ketamine is fundamentally different. It targets the glutamate system—the brain's primary excitatory neurotransmitter—to produce rapid changes in mood, cognition, and pain processing.

  • Traditional antidepressants: target serotonin/norepinephrine (weeks to work)
  • Ketamine: targets glutamate/NMDA receptors (hours to work)
  • Promotes new synaptic connections (synaptogenesis) rather than just adjusting neurotransmitter levels
  • Can provide relief even when all other medications have failed
  • Opens a window for therapeutic change through enhanced neuroplasticity

The NMDA Receptor Connection

Ketamine is classified as an NMDA receptor antagonist. NMDA receptors are a type of glutamate receptor involved in learning, memory, and neuroplasticity. By temporarily blocking these receptors, ketamine triggers a cascade of downstream effects that promote brain healing.

  • NMDA receptor blockade leads to a burst of glutamate release
  • This glutamate surge activates AMPA receptors
  • AMPA activation triggers mTOR signaling pathway
  • mTOR promotes rapid production of synaptic proteins
  • New synaptic connections form within hours—"rewiring" the brain

Neuroplasticity: The Key to Lasting Change

Depression, anxiety, and PTSD are associated with reduced neuroplasticity—the brain's ability to form new connections and adapt. Stress and trauma can cause synaptic atrophy, particularly in the prefrontal cortex. Ketamine reverses this by rapidly promoting synaptogenesis.

  • Increases BDNF (brain-derived neurotrophic factor)—the brain's "fertilizer"
  • Restores synaptic density in the prefrontal cortex within 24 hours
  • Reverses stress-induced neural atrophy
  • Creates a window of enhanced plasticity for therapeutic integration
  • Effects are synergistic with psychotherapy and integration practices

Sublingual Administration

Our at-home ketamine therapy uses sublingual (under-the-tongue) administration. This route provides effective blood levels while being safe for home use under medical supervision.

  • Tablet dissolves under the tongue for absorption through oral mucosa
  • Onset of effects typically within 10-20 minutes
  • Peak effects at 40-60 minutes, total duration 2-3 hours
  • Lower bioavailability than IV (30% vs 100%) but more sustained levels
  • Safer for at-home use with proper medical oversight
  • Dosing individualized by your physician based on response

Key Research Behind Ketamine Therapy

The landmark study that first demonstrated ketamine's rapid antidepressant effects in humans, sparking two decades of research. (Berman et al., 2000 (Biological Psychiatry))

Revealed ketamine's mechanism of action: rapid synaptogenesis in the prefrontal cortex through mTOR pathway activation, explaining its fast-acting antidepressant effects. (Li et al., 2010 (Science))

Established the "synaptogenic hypothesis" of depression treatment—that rapid restoration of synaptic connections underlies ketamine's antidepressant effects. (Duman & Aghajanian, 2012 (Science))

Frequently Asked Questions

How is ketamine different from traditional antidepressants?

Traditional antidepressants (SSRIs, SNRIs) increase serotonin or norepinephrine levels, taking 4-6 weeks to show effects. Ketamine targets the glutamate system and NMDA receptors, producing effects within hours. It also directly promotes the growth of new synaptic connections, rather than just adjusting neurotransmitter levels.

Is ketamine the same as esketamine (Spravato)?

Ketamine (racemic ketamine) contains two mirror-image molecules: S-ketamine and R-ketamine. Esketamine (Spravato) is only the S-isomer, delivered as a nasal spray in certified clinics. Our treatment uses racemic ketamine in sublingual form, which contains both isomers and may offer complementary benefits.

What does "subanesthetic" dose mean?

Ketamine was originally developed as an anesthetic at high doses. The doses used for depression, anxiety, and pain treatment are much lower—typically 10-25% of anesthetic doses. At these "subanesthetic" levels, patients remain conscious and can communicate, while still experiencing therapeutic effects.

How long do the neuroplasticity effects last?

The window of enhanced neuroplasticity typically lasts 24-72 hours after a session. This is why integration practices (journaling, reflection, therapy) during this window are so important. Repeated sessions can produce cumulative and longer-lasting changes in neural connectivity.

Can I feel the ketamine working in my brain?

During a session, you may experience altered perceptions, a sense of floating, mild dissociation, and emotional or visual experiences. These effects reflect the temporary changes in brain activity, particularly in the default mode network. They typically resolve within 1-2 hours after the session.

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