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Psilocin (4-hydroxy-N,N-dimethyltryptamine) is the active tryptamine responsible for the effects of psilocybin mushrooms, formed in the body when psilocybin is dephosphorylated after ingestion. Structurally a close relative of serotonin, it acts as an agonist or partial agonist at serotonin 5-HT2A receptors, the defining target of the classic psychedelics, with additional activity at 5-HT2C and 5-HT1A subtypes. Its lipophilicity lets it cross the blood-brain barrier readily and reach the brain within minutes, producing a psychedelic experience lasting several hours. Beyond acute receptor signaling, psilocin promotes markers of neuronal plasticity, and a compelling recent finding is that lipophilic psychedelics like psilocin can reach intracellular 5-HT2A receptors that serotonin itself cannot access, a mechanism proposed to underlie their durable therapeutic effects. It is the molecule that ultimately mediates psilocybin's clinical antidepressant activity.
- The active molecule that delivers psilocybin's psychedelic and therapeutic effects
- Crosses into the brain rapidly for a several-hour experience
- Promotes markers of neuronal plasticity
- Can reach intracellular 5-HT2A receptors that serotonin cannot access
- Nausea and pupil dilation
- Anxiety or difficult experiences during the acute phase
- Transient increases in heart rate and blood pressure
- Serotonergic cardiovascular caution in heart disease
- Strong potentiation if combined with MAO inhibitors
Mechanism
Psilocin is the pharmacologically active species behind the psilocybin experience. It is a substituted tryptamine that closely resembles and acts principally as an or partial agonist at serotonin receptors, while also engaging 5-HT2C and receptors; studies in animals confirm that 5-HT2A activation dominates the psychedelic response, with 5-HT1A and 5-HT2B/2C receptors modulating locomotor and behavioral components. Agonism at 5-HT2A receptors on cortical pyramidal neurons drives the changes in cortical excitability and network dynamics characteristic of psychedelics. Because psilocin is , it partitions readily into neuronal membranes and crosses the rapidly, and molecular dynamics work indicates that its membrane interactions differ subtly from serotonin's owing to its tertiary rather than primary amine.
The most distinctive facet of psilocin's mechanism concerns . Emerging evidence indicates that its enduring effects involve not only classical cell-surface signaling but biased agonism, engagement of intracellular 5-HT2A receptor pools that psychedelics can reach but membrane-impermeant cannot, and downstream activation of neurotrophic signaling including the receptor . This intracellular access has been proposed as a key reason psychedelics promote lasting neuroplastic remodeling that plain serotonin does not. Pharmacokinetically, psilocin reaches peak plasma and brain levels rapidly and dose-dependently after psilocybin ingestion, is metabolized by Phase I and Phase II pathways, principally glucuronidation to psilocin-O-glucuronide, the major urinary , and has an elimination of approximately two to three hours, consistent with a several-hour experience.
receptor fingerprint
receptoragonist / partial agonist
5-HT2C receptoragonist
receptoragonist
Intracellular pools / signalingactivation (lipophilic access)
Safetyrisks and cautions, not medical advice
Psilocin shares the generally favorable physiological safety profile of psilocybin, since it is the same active agent, with low toxicity and low addictive potential in supervised contexts. Common acute effects include nausea, pupil dilation, modest increases in heart rate and blood pressure, and the potential for anxiety or frightening experiences during the acute phase. As a direct 5-HT2A and 5-HT2B agonist it carries the serotonergic cardiovascular cautions of the class and should be avoided by people with serious cardiovascular disease.
It is contraindicated in those with a personal or family history of psychotic illness, and it should not be combined with monoamine oxidase inhibitors, which can markedly potentiate and prolong tryptamine effects, or with other serotonergic agents. Because psilocin is the active form, ingesting fresh or unprocessed mushroom material delivers it more directly and less predictably than standardized psilocybin. It is a controlled substance in most jurisdictions. Not medical advice.
Subjective profileweighing the evidence above
Physiologically it is the same agent as psilocybin, which has the best safety record among the classic psychedelics, but taking it directly removes the buffer the prodrug provides and it is a controlled substance nearly everywhere. Off the table with serious heart disease or a psychosis history, and never with an MAOI.
Resources
No suppliers are provided for compounds like this. This entry is here for reference.
Research
- 2007first citedHallucinogens recruit specific cortical 5-HT(2A) receptor-mediated signaling pathways to affect…
- 2025most active year4 papers
- 2026most recentNetwork pharmacology and molecular simulation reveal the entourage effect mechanisms of psilocy…
- 1.Emerging mechanisms of psilocybin-induced neuroplasticity
- 2.Possible psychedelic therapeutic mechanism
- 3.Metabolism of psilocybin and psilocin: clinical and forensic toxicological relevance
- 4.Pharmacokinetics of Psilocybin, a Tryptamine Alkaloid in Magic Mushroom (Psilocybe cubensis): A Systematic Review.
- 5.Acute psilocybin and ketanserin effects on cerebral blood flow: 5-HT2AR neuromodulation in healthy humans
- 6.Sex differences and serotonergic mechanisms in the behavioural effects of psilocin
- 7.Magic mushroom extracts in lipid membranes
- 8.Interaction of psychedelic tryptamine derivatives with a lipid bilayer
- 9.Network pharmacology and molecular simulation reveal the entourage effect mechanisms of psilocybin-producing mushrooms on the brain
- 10.Hallucinogens and Serotonin 5-HT2A Receptor-Mediated Signaling Pathways
- 11.Hallucinogens recruit specific cortical 5-HT(2A) receptor-mediated signaling pathways to affect behavior
- 12.5-HT2A receptors: Pharmacology and functional selectivity
12 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
How is psilocin different from psilocybin?
Psilocin is the active drug; psilocybin is the stable prodrug that the body converts into psilocin. When you take psilocybin, an enzyme removes a phosphate group to release psilocin, which is what actually enters the brain and produces the effects. Fresh mushrooms contain both.
What makes psilocin interesting to neuroscientists?
Beyond activating 5-HT2A receptors on the cell surface, psilocin is lipophilic enough to slip inside neurons and reach intracellular 5-HT2A receptors that the body's own serotonin cannot get to. This intracellular access, along with downstream TrkB and neurotrophic signaling, is a leading explanation for why psychedelics can promote durable neuroplastic changes.
Why does psilocin degrade so easily?
Psilocin is chemically less stable than psilocybin and oxidizes readily, which is why dried mushrooms and standardized psilocybin are preferred for consistent dosing. In the body it is cleared quickly, with a half-life of about two to three hours.
Adverse effects
- Nausea and pupil dilation
- Anxiety or difficult experiences during the acute phase
- Transient increases in heart rate and blood pressure
- Serotonergic cardiovascular caution in heart disease
- Strong potentiation if combined with MAO inhibitors