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Amanita muscaria
Fly agaric (Amanita muscaria, Amanitaceae) is a psychoactive fungus treated here as a whole-organism substance. Its primary psychoactive constituent, muscimol, is pharmacologically distinct from serotonergic psychedelics such as psilocybin. Muscimol activates GABA receptors throughout the brain, producing widespread neuronal inhibition that underlies its sedative-hallucinogenic character.[1]
Fly agaric (Amanita muscaria (L.) Lam., Amanitaceae) is a psychoactive basidiomycete fungus — not a plant, but treated here as a plant-type substance due to its whole-organism consumption pattern. Its primary psychoactive constituent, muscimol, is a selective GABA-A receptor agonist pharmacologically distinct from serotonergic psychedelics.[1] Muscimol produces its principal effects by activating GABA-A receptors throughout the brain, generating widespread neuronal inhibition that underlies the characteristic sedative-hallucinogenic experience.
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Siberian indigenous peoples consumed the mushroom for ritual trance and divination, with linguistic evidence suggesting use dating to approximately 4000 BCE.[2] Western researchers isolated muscimol and ibotenic acid in the 1960s,[3] yet no controlled clinical trials have been published for any preparation.[4] A commercial US market for muscimol products emerged around 2022–2023, leading the FDA to prohibit A. muscaria in conventional food products in December 2024.[5]
Subjective effects include sedation, perceptual distortion, dreamlike imagery, euphoria, ataxia, and confusion. The experience is characteristically biphasic — initial stimulation gives way to a dreamy, sedative state as the alkaloid balance shifts — with preparation method heavily determining the character.[6] Nausea, anxiety, and disorientation are commonly reported, particularly with fresh or minimally processed material.[4]
Fatal poisoning is exceedingly rare,[7] though severe intoxications involving coma and prolonged psychosis have been documented.[8][9] Combining muscimol with alcohol, benzodiazepines, or other sedatives can compound sedation and suppress breathing to a dangerous degree. No controlled human studies have been published and no clinical data on tolerance or dependence exist — an unusually sparse evidence base for a substance now widely sold commercially.
History[edit]
Traditional and historical use
A. muscaria has one of the longest documented histories of psychoactive use of any organism. Linguistic analysis of North Asian languages suggests consumption dating to approximately 4000 BCE.[6] Siberian indigenous peoples — including the Koryak, Chukchi, and Vogul — consumed dried fruiting bodies or infusions for ritual trance and divination.[6][2]
A documented traditional practice involved drinking the urine of someone who had consumed the mushroom. Muscimol passes through the body largely unmetabolized while ibotenic acid undergoes partial breakdown, yielding a preparation with a better muscimol-to-ibotenic acid ratio and lower gastrointestinal toxicity.[7][6]
Western discovery and modern era
Carl Linnaeus first described the species in 1753; muscimol and ibotenic acid were isolated in the 1960s.[3] A commercial US market for muscimol gummies, extracts, and vapes emerged around 2022–2023, with internet searches for A. muscaria rising 114% over that period.[10] The FDA prohibited the mushroom in conventional food products in December 2024.[5]
In 1968, R.G. Wasson proposed in Soma: Divine Mushroom of Immortality that A. muscaria was the Vedic soma referenced in the Rigveda.[11] The hypothesis is widely discussed in ethnomycological literature but contested by most Vedic scholars. North American indigenous use has also been documented among the Ojibwa and other groups.[6]
Botanical Overview[edit]
Taxonomy and classification
Amanita muscaria (L.) Lam. belongs to the family Amanitaceae. First described by Linnaeus in 1753 and moved to Amanita by Lamarck in 1783,[12] it is among the most recognized fungi in the world. Several varieties exist — including red-capped Eurasian and North American forms and yellow-orange forms — with some variation in alkaloid concentration across varieties. citation needed
Range and habitat
The mushroom is native to temperate and boreal forests across the Northern Hemisphere, growing in association with birch, pine, spruce, and fir. It has spread to Australia, New Zealand, and parts of South America through forestry plantations. Fruiting bodies appear from late summer through autumn.
Identification
The classic form features a bright red to orange-red cap, 8–20 cm across, with white warts and a ringed white stipe. Yellow-capped varieties can be confused with A. pantherina (higher alkaloid load). More dangerously, inexperienced foragers may mistake Amanita species for A. phalloides (death cap) — lethally toxic. Professional mycological verification is essential for wild-harvested material.
Alkaloid Profile[edit]
Dominant alkaloids
The psychoactive character of A. muscaria comes from two compounds. Muscimol is the principal active alkaloid — a GABA agonist producing sedation and hallucinogenic effects.[1] Ibotenic acid is its chemical precursor: it activates glutamate receptors, driving excitation, and is potentially damaging to neurons at high concentrations.[7]
Ratio and pharmacokinetics
The ratio between these alkaloids determines the character of the experience. Fresh material runs approximately 9:1 ibotenic acid-to-muscimol; drying shifts it toward 3:2.[6] In the body, 10–50% of ingested ibotenic acid converts further to muscimol.[13] Both compounds are rapidly absorbed and excreted largely unmetabolized via the kidneys[14][7] — the physiological basis for the ethnographically documented urine-recycling practice.
Minor alkaloids and variability
Muscarine — the compound behind the species name — is present only in trace amounts. It causes salivation and sweating but contributes little to the central experience.[15] citation needed Alkaloid concentrations vary significantly across specimens, varieties, and harvest conditions; commercial products cannot guarantee consistent content,[10] making precise dosing inherently unreliable.
Neuroscience[edit]
Where it acts
Muscimol activates GABA-A receptors throughout the brain — especially extrasynaptic receptors that sustain prolonged inhibition — producing widespread CNS depression.[1] Ibotenic acid simultaneously activates glutamate receptors, driving excitation and, at high concentrations, potential cellular damage.[7] Secondary effects include elevated serotonin and reduced catecholamine levels.[13][16]
What it changes
The biphasic experience maps to this interplay: ibotenic acid drives the initial excitatory phase, while muscimol — accumulating as decarboxylation proceeds — produces the dreamy, sedative state.[6] The hallucinogenic quality — size distortions, visual warping, dreamlike imagery — arises from muscimol disrupting the brain's thalamic filtering system. Unlike serotonergic psychedelics, this is neuronal suppression, not amplification.
- No published human neuroimaging studies (fMRI, PET, or EEG) exist for A. muscaria or muscimol
- The specific contribution of extrasynaptic versus synaptic GABA-A receptor activation to the subjective experience remains uncharacterized
- Whether chronic muscimol exposure produces the same downregulation and tolerance seen with benzodiazepines or barbiturates has not been studied
Subjective Effects[edit]
The A. muscaria experience is fundamentally sedative-hallucinogenic in character — closer to a dreamlike twilight state than to the perceptual amplification of serotonergic psychedelics. Fresh material skews excitatory and nauseating; dried and heat-processed preparations favor the sedative-oneiric quality the substance is known for.[6] Set and setting shape the psychological tone substantially — the balance between tranquility and anxiety is particularly sensitive.
At higher doses, A. muscaria sits closer to deliriant substances than to classical psychedelics. Reality testing becomes impaired, amnesia is prominent, and insight — typically preserved with serotonergic psychedelics at moderate doses — is not reliable.[4] Its GABA-A mechanism distinguishes it from both anticholinergic delirium and serotonergic expansion.
Siberian shamanic use of A. muscaria dates back millennia, with linguistic evidence suggesting consumption as early as 4000 BCE.[2] Western science isolated its key alkaloids in the 1960s,[3] yet no controlled clinical trials have been published for any preparation.[4] A commercial market for muscimol products emerged in the US circa 2022–2023, prompting the FDA to prohibit A. muscaria in conventional food products in December 2024.[5]
Subjective effects include sedation, perceptual distortion, oneiric imagery, euphoria, ataxia, and confusion. The experience is characteristically biphasic — initial stimulation from ibotenic acid gives way to a dreamy, sedative state as decarboxylation to muscimol proceeds — with preparation method heavily determining the balance.[6] Nausea, anxiety, disorientation, and impaired reality testing are commonly reported, particularly with fresh or minimally processed material.[4]
Fatal poisoning is exceedingly rare,[7] though severe intoxications involving coma and prolonged psychosis have been documented.[8][9] No published data exist on tolerance, dependence, or withdrawal — a significant gap given muscimol's mechanistic parallels to benzodiazepine pharmacology. Heavy metal contamination in commercial preparations[10] and the complete absence of controlled human studies define an unusually sparse evidence base for a substance with growing commercial availability.
History[edit]
Traditional and historical use
A. muscaria has one of the longest documented histories of psychoactive use of any organism. Linguistic analysis of North Asian languages suggests consumption dating to approximately 4000 BCE,[6] and Paleolithic Saharan rock paintings have been interpreted — controversially — as depicting mushroom figures.[6]
Siberian shamanic use is the best-documented traditional application. Multiple indigenous peoples — including the Koryak, Chukchi, Kamchadal, Ostyak, and Vogul — consumed dried fruiting bodies or liquid infusions for ritual intoxication, trance, and divination.[6][2] A distinctive documented practice involved drinking the urine of individuals who had consumed the mushroom: muscimol passes through the body largely intact while ibotenic acid undergoes partial metabolism, yielding a preparation with a more favorable muscimol-to-ibotenic acid ratio and reduced gastrointestinal toxicity.[7][6]
Western discovery and research
Carl Linnaeus first described the species as Agaricus muscarius in Species Plantarum (1753); Jean-Baptiste Lamarck transferred it to Amanita in 1783.[11] The common name "fly agaric" derives from the European practice of placing the cap in milk to attract and kill flies.[3]
Ibotenic acid and muscimol were isolated and characterized in the 1960s.[3] Michelot and Melendez-Howell produced the most comprehensive integrated review of A. muscaria chemistry, biology, and toxicology in 2003.[3] Li and Oberlies catalogued the natural products of the entire Amanita genus in 2005.[12]
Modern era
A commercial market for muscimol-containing products — gummies, extracts, vapes, and pre-rolls — emerged in the United States circa 2022–2023. Google searches for A. muscaria increased 114% from 2022 to 2023, exceeding expected seasonal trends by 97.4%.[13] The FDA issued a formal letter in December 2024 prohibiting the mushroom and its constituents in conventional food products.[5]
The first UK hospitalization from a commercial A. muscaria product — linked to a microdosing regimen — was reported in July 2023.[5] Hartwig et al. published the first academic thematic analysis of community user experiences in 2025.[4] Louisiana became the only US state to explicitly restrict A. muscaria for human consumption (2005),[14] with the Netherlands banning it in 2008 and Romania in 2010.[6][14]
In 1968, R.G. Wasson proposed in Soma: Divine Mushroom of Immortality that A. muscaria was the identity of the Vedic soma referenced in the Rigveda.[15] The hypothesis remains widely discussed in ethnomycological literature but is contested by most scholars in Vedic studies. North American indigenous use has been documented among the Ojibwa and other groups.[6]
Botanical Overview[edit]
Taxonomy and classification
Amanita muscaria (L.) Lam. belongs to the family Amanitaceae within the order Agaricales (phylum Basidiomycota). First described by Linnaeus as Agaricus muscarius in 1753 and transferred to Amanita by Lamarck in 1783,[11] it is among the most widely recognized fungi in the world. Several varieties are recognized — including var. muscaria (Eurasian red-capped form), var. flavivolvata (North American red-capped), var. guessowii (yellow-orange cap), and var. formosa — with variation in cap color and potentially in alkaloid concentration. citation needed
Range and habitat
A. muscaria is native to temperate and boreal forests throughout the Northern Hemisphere, forming ectomycorrhizal associations primarily with birch, pine, spruce, and fir. It has been introduced to the Southern Hemisphere — including Australia, New Zealand, and parts of South America — through forestry plantations of its host trees. Fruiting bodies typically appear in late summer through autumn.
Identification
The classic form is distinctive: a bright red to orange-red cap (pileus), 8–20 cm in diameter, covered with white to yellowish remnants of the universal veil (warts). The stipe is white with a bulbous base and a skirt-like ring (annulus). Gills are white and free from the stipe.
Critical identification caution: yellow- and orange-capped varieties of A. muscaria can be confused with A. pantherina (panther cap), which contains the same isoxazole alkaloids at higher concentrations. More dangerously, inexperienced foragers may confuse Amanita species with lethal amatoxin-containing species such as A. phalloides (death cap) or A. virosa (destroying angel). Professional mycological verification is essential for wild-harvested material.
Harvesting and processing
Fruiting bodies are harvested whole. The critical processing step is drying, which drives the decarboxylation of ibotenic acid to muscimol — shifting the alkaloid ratio from approximately 9:1 (ibotenic acid-dominant in fresh material) toward 3:2.[6] This conversion substantially changes the pharmacological character and tolerability of the preparation. Detailed preparation methods are described in the Preparations section.
Alkaloid Profile[edit]
Dominant alkaloids
The psychoactive properties of A. muscaria derive from two isoxazole compounds. muscimol is the principal active alkaloid, a selective GABA-A receptor agonist that produces the characteristic sedative-hallucinogenic experience.[1] Ibotenic acid, muscimol's metabolic precursor, is a non-selective NMDA and metabotropic glutamate receptor agonist with excitatory and neurotoxic properties.[7]
The ratio between these two alkaloids is the primary variable determining the pharmacological character of any A. muscaria preparation. Fresh material contains ibotenic acid and muscimol at approximately 9:1. Drying shifts this ratio toward approximately 3:2 as ibotenic acid decarboxylates to muscimol.[6] In vivo, approximately 10–50% of ingested ibotenic acid undergoes decarboxylation to muscimol.[10]
Minor alkaloid
Muscarine, the compound from which the species derives its name, is present at trace concentrations. It activates muscarinic cholinergic receptors peripherally, producing salivation, lacrimation, and sweating, but its contribution to the central psychoactive experience is negligible.[16] Despite the name, A. muscaria contains far less muscarine than other species such as certain Inocybe and Clitocybe fungi. citation needed
Variability
Alkaloid concentrations vary significantly across specimens, varieties, geographic origin, and harvest conditions. Cap tissue generally contains higher concentrations than stipe material. No standardized quantification protocol exists for commercial products, and commercial preparations cannot guarantee consistent alkaloid content.[13] This variability makes precise dosing from whole-mushroom preparations inherently unreliable.
Pharmacokinetics
Both ibotenic acid and muscimol are rapidly absorbed from the gastrointestinal tract and appear in urine within 20–90 minutes of ingestion.[17][7] Both compounds are excreted substantially unmetabolized via the kidneys[17] — this property is the physiological basis for the ethnographically documented urine-recycling practice. No published data exist on CYP enzyme involvement in the metabolism of either compound.
Neuroscience[edit]
Where it acts
The A. muscaria experience arises from the interplay of two opposing neurotransmitter systems. Muscimol activates ionotropic GABA-A receptors — particularly high-efficacy extrasynaptic receptors that mediate tonic (sustained) inhibition — producing broad CNS depression.[1] Secondary neurochemical effects include increased serotonin and decreased catecholamine levels.[10][18] Ibotenic acid, meanwhile, activates NMDA and metabotropic glutamate receptors, producing excitatory effects[7] and, at high concentrations, excitotoxic damage via calcium influx.[10]
What it changes
The biphasic temporal profile maps directly to the transition from ibotenic acid excitation to muscimol-dominant inhibition as decarboxylation proceeds in vivo.[6] Fresh preparations produce more initial agitation and gastrointestinal distress; dried preparations favor sedation and oneiric states.
The hallucinogenic quality — macropsia, micropsia, visual distortion, dreamlike imagery — arises from muscimol's modulation of thalamocortical circuits. Unlike serotonergic psychedelics acting at 5-HT₂A receptors, GABA-A agonism disrupts sensory gating and thalamic filtering rather than producing cortical hyperconnectivity.
- No published human neuroimaging studies (fMRI, PET, or EEG) exist for A. muscaria or muscimol
- The specific contribution of extrasynaptic versus synaptic GABA-A receptor activation to the subjective experience remains uncharacterized
- Whether chronic muscimol exposure produces the same downregulation and tolerance seen with other GABA-A agonists (benzodiazepines, barbiturates) has not been studied
Subjective Effects[edit]
The A. muscaria experience is fundamentally GABAergic in character — a dreamy, sedative state resembling twilight consciousness more than the perceptual amplification of tryptamine or phenethylamine psychedelics. The experience is heavily preparation-dependent: fresh material skews excitatory and gastrointestinally aversive, while dried and heat-processed preparations favor the sedative-oneiric quality that defines the substance's reputation.[6] Set and setting modulate the psychological dimensions substantially — particularly the balance between tranquility and anxiety.
Phenomenologically, A. muscaria sits closer to deliriant substances than to classical psychedelics, especially at higher doses where reality testing is impaired and amnesia is prominent.[4] Its mechanism (GABA-A agonism) is distinct from both anticholinergic and serotonergic classes. The closest pharmacological comparator is gaboxadol (THIP), a synthetic muscimol structural analog that was studied in clinical trials for insomnia.
Effect Grid
At 8–10 g dried cap (~10–15 mg muscimol), the characteristic biphasic pattern emerges. Initial stimulation from ibotenic acid gives way to muscimol-dominant sedation and dreaming enhancement. Perspective distortion — particularly visual magnification (macropsia) and its inverse (micropsia) — is the signature perceptual effect. Internal hallucinations with oneiric, dreamlike imagery are common. Auditory distortion and auditory hallucinations may occur. Cognitive euphoria alternates with anxiety. Analysis suppression, memory suppression, and partial amnesia for portions of the experience are typical.
Nausea affects the majority of users and may progress to vomiting. Sedation is pronounced. Motor control impairment produces visible ataxia and dizziness. Excessive sweating, salivation, and involuntary body movements (muscle jerks) reflect the mixed GABAergic-glutamatergic pharmacology. Confusion and temporal disorientation are common.
Expect a 6-hour primary commitment with 10–24 hours of residual cognitive fog, physical fatigue, and grogginess. Do not drive or operate machinery for at least 24 hours.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Perspective distortion · Spatial disorientation · Vestibular distortion · Visual haze / noise · Color alteration · Visual drifting · Auditory distortion · Visual acuity suppression · Proprioceptive distortion · After-images · Tracers · Peripheral misidentification · Music enhancement · Color enhancement · Auditory enhancement · Auditory misinterpretation · Brightness alteration · Peripheral vision distortion · Visual breathing · Visual morphing · Synesthesia · Visual melting · Visual acuity enhancement · Internal hallucinations · External hallucinations · Object transformations · Auditory hallucinations · Object activation · Perspective hallucinations · Visual processing suppression · Visual recursion
Color alteration · Visual drifting · Auditory distortion · Visual acuity suppression · Proprioceptive distortion · After-images · Tracers · Peripheral misidentification · Music enhancement · Color enhancement · Auditory enhancement · Auditory misinterpretation · Brightness alteration · Peripheral vision distortion · Visual breathing · Visual morphing · Synesthesia · Visual melting · Visual acuity enhancement · Internal hallucinations · External hallucinations · Object transformations · Auditory hallucinations · Object activation · Perspective hallucinations · Visual processing suppression · Visual recursion
Dizziness · Physical fatigue · Pupil constriction · Salivation · Bodily heaviness · Body high · Body schema distortion · Sexual arousal suppression · Spontaneous body sensations · Excessive sweating · Pain suppression · Appetite suppression · Vomiting · Involuntary body movements · Nystagmus (eye wobbles) · Bodily lightness · Headache · Trembling · Watery eyes · Pupil dilation · Stimulation · Breathing alteration · Heart rate perception changes · Laughter fits · Restlessness · Tactile euphoria · Tingling / electric sensations · Bodily dissociation · Tactile hallucination
Bodily heaviness · Body high · Body schema distortion · Sexual arousal suppression · Spontaneous body sensations · Excessive sweating · Pain suppression · Appetite suppression · Vomiting · Involuntary body movements · Nystagmus (eye wobbles) · Bodily lightness · Headache · Trembling · Watery eyes · Pupil dilation · Stimulation · Breathing alteration · Heart rate perception changes · Laughter fits · Restlessness · Tactile euphoria · Tingling / electric sensations · Bodily dissociation · Tactile hallucination
Immersion enhancement · Memory suppression · Information processing suppression · Memory fragmentation · Motivation suppression · Thought deceleration · Thought disorganization · Cognitive euphoria · Analysis suppression · Introspection enhancement · Focus suppression · Language suppression · Aesthetic enhancement · Cognitive dysphoria · Creativity suppression · Increased nature relatedness · Openness enhancement · Pattern recognition suppression · Thought loops · Creativity enhancement · Analysis enhancement · Humor enhancement · Amnesia · Delirium · Delusions
Memory fragmentation · Motivation suppression · Thought deceleration · Thought disorganization · Cognitive euphoria · Analysis suppression · Introspection enhancement · Focus suppression · Language suppression · Aesthetic enhancement · Cognitive dysphoria · Creativity suppression · Increased nature relatedness · Openness enhancement · Pattern recognition suppression · Thought loops · Creativity enhancement · Analysis enhancement · Humor enhancement · Delirium · Delusions
Emotional enhancement · Emotional lability · Emotional suppression · Empathy enhancement · Catharsis · Irritability · Simultaneous emotions
Catharsis · Irritability · Simultaneous emotions
Emotional susceptibility · Sociability suppression · Social disconnection · Ego inflation · Sociability enhancement · Cognitive disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Sociability enhancement · Cognitive disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Entity contact · Non-dual awareness · Voidness · Death-rebirth sequence · Near-death experience
Near-death experience
Preparations[edit]
Preparation method is the most important variable in the A. muscaria experience. Drying drives conversion of ibotenic acid to muscimol — shifting the alkaloid balance from excitatory and nauseating toward sedative and hallucinogenic.[6] Potency varies significantly across specimens, varieties, and harvest conditions;[10] all dose ranges below are approximate.
Dried cap (oral)
Dried cap is the traditional preparation and the most common. Drying shifts the ibotenic acid-to-muscimol ratio from approximately 9:1 (fresh) toward 3:2.[6] Onset: 30–90 minutes after ingestion.[7] Peak: 2–3 hours. Primary duration: approximately 6 hours. Residual effects: 10–24 hours.[7] The experience favors sedation, perceptual distortion, and dreamlike imagery.
Tea / aqueous infusion (oral)
Tea (hot water extraction of dried cap material) extracts the water-soluble alkaloids; straining removes indigestible chitin. This preparation may reduce gastrointestinal distress compared to consuming dried mushroom directly. Onset and duration are comparable to dried cap. No standardized extraction efficiency data exist — potency per cup is unpredictable. citation needed
Fresh fruiting body (oral)
Fresh fruiting body retains the approximately 9:1 ibotenic acid-to-muscimol ratio[6] and carries the highest gastrointestinal toxicity burden. Initial effects are excitatory — agitation, nausea, confusion — before shifting toward sedation. This preparation carries elevated risk and is not recommended for intentional use.
Commercial products (gummies, extracts, vapes)
Commercial muscimol products emerged in the US market around 2022–2023.[10] No standardized testing or dosing protocols exist.[10] Cadmium contamination exceeding permissible limits by 4–9× has been documented in tested preparations.[13] The FDA has prohibited A. muscaria in conventional food products.[5]
Per-preparation dose tiers, timelines, and bioavailability data are in the Dose · by preparation card on this page.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- unknown
- Tolerance reset
- —
- Physical
- Negligible
- Psychological
- Low
- Compulsive redosing
- Low
- Dose escalation
- Low
- Cross-tol.
- benzodiazepines · barbiturates · gaboxadol (THIP)
○ not assessed: TOL
Toxicity
Fatal poisoning is exceedingly rare.[7] One confirmed fatality is documented — a man who ingested four dried caps.[10] The clinical syndrome (pantherina-muscaria syndrome[17][3]) begins 30–90 minutes after ingestion (up to 180 minutes in children[18]) and includes confusion, ataxia, hallucinations, nausea, and sweating. Severe cases can produce coma,[9][17] seizures, and respiratory failure. Atropine is not indicated and does not address the underlying mechanism.[7][18] Commercial preparations have shown cadmium at 4–9× permissible limits and lead at near-threshold levels;[13] no standardized testing program exists.[10] Ibotenic acid carries theoretical neurotoxicity risk at high concentrations.[13] Misidentification with lethally toxic species (A. phalloides, A. virosa) is an additional unregulated supply-chain risk.
Psychological Risks
Anxiety, paranoia, confusion, and disorientation are common at moderate-to-high doses.[4] Most adverse psychological effects are self-limiting,[4] but more severe outcomes occur. Prolonged psychosis lasting five days — with visual and auditory hallucinations and paranoid ideation, beginning 18 hours after ingestion — has been documented.[8] In a case series of five young recreational users, four experienced hallucinations and all recovered within four days.[19] The deliriant character at higher doses — impaired reality testing and amnesia — poses psychological risk that serotonergic psychedelics at moderate doses do not.
Tolerance & Dependence
No clinical data exist on tolerance development, dependence, or withdrawal specific to muscimol or A. muscaria. Community reports suggest it is not compulsively used.[13][4] However, muscimol activates the same receptor class as benzodiazepines — a drug class that produces physical dependence and a withdrawal syndrome with chronic use. Whether muscimol carries analogous risks has not been studied. Commercial vendor claims that users can stop without difficulty lack any clinical evidence.
Drug Interactions
The most serious risk is additive sedation and respiratory depression with other GABAergic substances. Muscimol directly activates GABA-A receptors; combining it with any of the following deepens this effect[13][7]:
- Benzodiazepines (diazepam, alprazolam, clonazepam) — additive sedation and respiratory depression
- Barbiturates — additive CNS depression
- Alcohol — additive sedation, ataxia, respiratory depression
- Z-drugs (zolpidem, zopiclone) — additive sedation
- Gabapentinoids (gabapentin, pregabalin) — additive CNS depression
Ibotenic acid's glutamate receptor activity may compound seizure risk with tramadol, bupropion, or certain antipsychotics. Both compounds appear to undergo minimal liver metabolism,[14] suggesting low CYP-mediated interaction risk — though this has not been formally studied. safety citation needed
Contraindications
Specific populations face elevated risk:
- Children — seizures occurred in 4 of 9 pediatric cases in the largest published series.[18]
- Elderly — severe poisoning requiring hospitalization is documented.[17]
- Pregnancy — no reproductive toxicity data exist; muscimol's GABAergic mechanism raises theoretical concern for fetal brain development. safety citation needed
- Epilepsy or seizure disorders — ibotenic acid has excitotoxic and seizure-promoting properties.
- Psychotic disorders — prolonged psychosis has been documented following use.[8]
- Concurrent GABAergic medication (benzodiazepines, barbiturates, Z-drugs, gabapentinoids, alcohol) — additive CNS and respiratory depression risk.[7]
- Renal impairment — muscimol is excreted largely unmetabolized via the kidneys;[14] impaired renal function could prolong effects.
Harm Reduction[edit]
Forms & Identification
A. muscaria preparations in commerce — gummies, extracts, dried caps, and vape cartridges — lack standardized testing. Alkaloid concentrations vary dramatically across specimens and processing methods, and heavy metal contamination (cadmium, lead) exceeding permissible safety limits has been documented in tested products.
For whole dried mushroom, professional mycological verification is essential. Yellow and orange varieties can be confused with A. pantherina (higher alkaloid load) or, more dangerously, with lethally toxic species such as A. phalloides. For commercial products, request a Certificate of Analysis from a third-party laboratory showing alkaloid content and heavy metal testing.
Guidelines
- Start with dried, heat-processed material only. Fresh mushrooms retain an approximately 9:1 ibotenic acid-to-muscimol ratio and carry substantially higher gastrointestinal toxicity.
- Start low. Begin with the lowest suggested dose and wait at least 2 hours before considering any additional consumption. Onset can take up to 90 minutes.
- Test the source. Verify that commercial products come with third-party lab testing for alkaloid content and heavy metals. Products without a CoA should be treated as unknown-potency preparations.
- Never combine with alcohol, benzodiazepines, or other sedatives. Muscimol's GABA-A agonism creates additive CNS and respiratory depression with any GABAergic substance.
- Do not drive or operate machinery. Motor control impairment, confusion, and perceptual distortion make coordination dangerous.
- Have a sober companion present. Moderate-to-high doses may impair the ability to recognize an emergency or make sound decisions.
- Stay hydrated. Nausea and sweating are common. Maintain fluid intake throughout.
Set & Setting
The A. muscaria experience is unpredictable. The shift from initial excitation to deep sedation, the deliriant quality at higher doses, and the risk of impaired reality testing demand careful planning. Use only in a safe, familiar, private setting — no access to water, heights, or roads. A sober companion is strongly recommended.
This is not a clear-headed experience. Anticipate a dreamy, disorienting state closer to sleep than to serotonergic psychedelic insight. Anxiety is common, particularly during the initial excitatory phase.
Aftercare & integration. Residual effects — grogginess, confusion, and perceptual oddities — may persist for 10–24 hours after the primary experience. Plan for a full day of recovery with no obligations. Sleep is often disrupted.
Hydrate and eat lightly. Nausea may linger; bland foods and electrolyte drinks help. If significant anxiety or confusion persists beyond 24 hours, contact a healthcare provider.
The dreamlike, often fragmentary quality of the experience benefits from journaling within 24 hours. Memory of the experience is often partial or distorted — integration is more challenging than with serotonergic psychedelics.
Recovery & Support
No published data characterize a dependence or withdrawal specific to A. muscaria. Given muscimol's mechanistic parallels to benzodiazepines, individuals using preparations frequently or in escalating amounts should approach cessation with caution. If regular use has developed, taper gradually rather than stopping abruptly. Monitor for rebound effect anxiety, insomnia, or agitation.
For support:
- SAMHSA National Helpline: 1-800-662-4357 (US, free, confidential, 24/7)
- Crisis Text Line: Text HOME to 741741 (US)
- Poison Control: 1-800-222-1222 (US) for acute ingestion concerns
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Unresponsiveness or inability to be roused
- Breathing that is slow, shallow, or irregular
- Prolonged seizure activity
- Severe confusion with agitation or self-harm risk
- Vomiting while unconscious or semi-conscious
Immediate steps:
- 1. Call emergency services immediately if the person is unresponsive, seizing, or showing breathing difficulties.
- 2. Place an unconscious but breathing person in the recovery position (on their side) to protect the airway.
- 3. Do not induce vomiting.
- 4. Do not administer atropine — it does not address the central mechanism and is not indicated for A. muscaria poisoning.
- 5. Stay with the person. Monitor breathing continuously until help arrives.
What to tell the dispatcher:
State that the person ingested Amanita muscaria (fly agaric mushroom), the approximate amount and form (dried caps, tea, commercial product), the time of ingestion, and current symptoms. Good Samaritan laws exist in many jurisdictions and provide legal protection for those seeking emergency help.
No reversal agent exists for muscimol or ibotenic acid intoxication. Treatment is supportive.
Legal Status[edit]
A. muscaria, muscimol, and ibotenic acid are not listed under any United Nations drug control treaty — they fall outside the 1961, 1971, and 1988 conventions. Legal status is determined entirely by individual countries, producing a patchwork that ranges from unrestricted to outright prohibition.
In the United States, the mushroom is not scheduled under federal law, but the FDA prohibited it in conventional food products in December 2024.[5] Louisiana is the only US state with a confirmed explicit ban.[20] The Netherlands banned possession above threshold amounts in 2008, and Romania banned it in 2010.[6][20] Australia places it on Schedule 9 — prohibited except for approved research.[20] Germany and most EU countries do not specifically schedule the mushroom or its alkaloids.[13] Canada is unscheduled under the Controlled Drugs and Substances Act. citation needed The UK does not list it under the Misuse of Drugs Act 1971, though marketing for psychoactive purposes may invoke the Psychoactive Substances Act 2016.[20] Restrictions have been reported in Russia, Sweden, Ukraine, Thailand, and Brazil, but specific legislation in those jurisdictions has not been independently verified.[5] citation needed
Legal status changes frequently. This overview reflects status as of the article's last update and is not legal advice. Verify current law in the relevant jurisdiction before acting on this information.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- unknown
- Tolerance reset
- —
- Physical
- Negligible
- Psychological
- Low
- Compulsive redosing
- Low
- Dose escalation
- Low
- Cross-tol.
- benzodiazepines · barbiturates · gaboxadol (THIP)
○ not assessed: TOL
Toxicity
Fatal human poisoning from A. muscaria is exceedingly rare.[7] One confirmed fatality has been documented in a 44-year-old man who ingested four dried caps.[13] A "2–5% fatality rate" cited in one review[10] has not been confirmed by systematic analysis and may conflate A. muscaria data with lethal amatoxin-containing species. safety citation needed
The clinical toxidrome — the pantherina-muscaria syndrome — is well-characterized and distinct from amatoxin poisoning.[19][3] Onset occurs 30–90 minutes after ingestion (up to 180 minutes in children[20]). Mild-to-moderate presentations include CNS depression, confusion, ataxia, hallucinations, euphoria alternating with dysphoria, muscle jerks, nausea, and sweating. Severe intoxications may produce coma,[9][19] seizures (documented in 4 of 9 pediatric cases[20]), respiratory failure, and delirium.
Atropine is not recommended for A. muscaria poisoning and does not address the central GABAergic/glutamatergic mechanism.[7] Despite the presence of trace muscarine, the toxidrome does not present as a classic cholinergic or anticholinergic syndrome.[20]
Ibotenic acid is an established excitotoxin used experimentally to produce focal brain lesions via NMDA-mediated mechanisms.[10] No human cases of chronic ibotenic acid-induced neurotoxicity have been published, but this risk is theoretically relevant for repeated exposure to preparations with high ibotenic acid content.
Heavy metal contamination is a significant concern for commercial preparations. Cadmium levels in tested supplements exceeded permissible safety limits by 4–9×, and lead concentrations approached threshold values.[10] A. muscaria naturally bioaccumulates vanadium and other heavy metals from soil. No standardized laboratory testing program or Certificate of Analysis standard exists for A. muscaria products.[13] The FDA has not accepted GRAS or NDI notifications for muscimol.[5]
Misidentification of source material constitutes an additional risk: substitution with A. pantherina (higher alkaloid load) or confusion with amatoxin-containing species (potentially lethal) is possible in unregulated supply chains.
Psychological Risks
Anxiety, paranoia, confusion, and disorientation are commonly reported at moderate-to-high doses.[4] A community thematic analysis found most adverse psychological effects to be self-limiting,[4] but clinical case reports document more severe outcomes.
Prolonged psychosis lasting five days — with visual and auditory hallucinations and paranoid ideation, developing 18 hours after ingestion — has been documented.[8] In a case series of five young recreational users (ages 18–21), four experienced hallucinations and one lost consciousness; all recovered within four days.[21]
The deliriant character of higher-dose experiences — involving impaired reality testing and amnesia — carries psychological risk distinct from classical serotonergic psychedelics, where insight is typically preserved at moderate doses.
Tolerance & Dependence
No published clinical data exist on tolerance development, abuse liability, or withdrawal characterization specific to muscimol or A. muscaria. This is a significant data gap.
Community reports suggest A. muscaria is not compulsively used and has a non-addictive profile.[10][4] However, muscimol's GABAergic mechanism is mechanistically analogous to benzodiazepine pharmacology — a drug class that produces tolerance, physical dependence, and a withdrawal syndrome (rebound effect anxiety, insomnia, seizure risk) with chronic use. Whether chronic muscimol exposure carries analogous risks has not been studied. Claims from commercial vendors that users "can simply discontinue without unwanted effects" lack rigorous clinical support.
Drug Interactions
The most significant concern is additive CNS and respiratory depression with other GABAergic agents. Muscimol's direct GABA-A agonism creates a clear mechanistic basis for potentiation with:
- Benzodiazepines (diazepam, alprazolam, clonazepam) — additive sedation and respiratory depression
- Barbiturates — additive CNS depression
- Alcohol — additive sedation, ataxia, respiratory depression
- Z-drugs (zolpidem, zopiclone) — additive sedation
- Gabapentinoids (gabapentin, pregabalin) — additive CNS depression
Co-administration with any of these agents would be expected to potentiate sedation, respiratory depression, and coma risk.[10][7] No clinical case reports quantifying these specific interactions have been published. safety citation needed
Ibotenic acid's NMDA receptor agonism may compound seizure risk when combined with drugs that lower seizure threshold (tramadol, bupropion, certain antipsychotics).
No published data exist on CYP enzyme interactions for muscimol or ibotenic acid. Both compounds appear to undergo minimal hepatic metabolism,[17] suggesting low CYP-mediated interaction potential — but this has not been formally studied.
Contraindications
Pediatric use is contraindicated. Children demonstrate increased susceptibility to seizures: seizures occurred in 4 of 9 pediatric cases in the largest published series.[20]
Elderly populations show increased vulnerability to severe intoxication. Severe poisoning in elderly spouses requiring hospitalization has been documented.[19]
Pregnancy is an absolute contraindication. No reproductive toxicity data exist, but muscimol's GABAergic mechanism raises theoretical concern for fetal CNS development during the period when GABA transitions from excitatory to inhibitory signaling in the developing brain. safety citation needed
Epilepsy and seizure disorders are a relative contraindication due to ibotenic acid's excitotoxic and seizure-promoting properties.
Pre-existing psychotic disorders are a relative contraindication given documented prolonged psychosis[8] and the deliriant character of higher-dose experiences.
Concurrent GABAergic medication use (benzodiazepines, barbiturates, Z-drugs, gabapentinoids, alcohol) is a relative contraindication due to additive CNS and respiratory depression risk.
Renal impairment is a relative contraindication. Muscimol is excreted substantially unmetabolized via the kidneys;[17] impaired renal function could prolong effects and increase accumulation risk.
Preparations[edit]
Preparation method is the single most important variable in determining the pharmacological character, tolerability, and risk profile of an A. muscaria experience. The decarboxylation of ibotenic acid to muscimol — driven by heat and drying — shifts the alkaloid balance from excitatory and nauseating toward sedative and hallucinogenic.[6] Potency varies significantly across specimens, varieties, and harvest conditions;[13] all dose ranges below are approximate.
Dried cap (oral)
Dried cap is the traditional and most common preparation. Drying at low heat shifts the ibotenic acid-to-muscimol ratio from approximately 9:1 (fresh) toward 3:2.[6] Onset occurs 30–90 minutes after ingestion,[7] with peak effects at 2–3 hours, primary duration of approximately 6 hours, and residual effects persisting 10–24 hours.[7] The experience favors sedation, perceptual distortion, and oneiric imagery. Nausea remains possible but is reduced compared to fresh material.
Tea / aqueous infusion (oral)
Tea (hot water extraction of dried cap material) is a common preparation that may further reduce gastrointestinal distress compared to consuming dried mushroom directly. Simmering or steeping in hot water extracts the water-soluble isoxazole alkaloids; straining removes indigestible chitin. Onset and duration are comparable to dried cap consumption. No standardized extraction efficiency data exist — potency per cup is unpredictable. citation needed
Fresh fruiting body (oral)
Fresh fruiting body retains the approximately 9:1 ibotenic acid-to-muscimol ratio[6] and carries the highest gastrointestinal toxicity burden. Initial effects skew excitatory — agitation, nausea, and confusion — before shifting toward sedation as ibotenic acid decarboxylates in vivo. This preparation carries elevated risk of adverse effects and is not recommended for intentional use.
Commercial products (gummies, extracts, vapes)
Commercial muscimol products — gummies, liquid extracts, and vape cartridges — emerged in the US market circa 2022–2023.[13] No standardized testing or dosing protocols exist for these products.[13] Labeling accuracy is unverified: stated muscimol content may not reflect actual concentration. Heavy metal contamination — particularly cadmium exceeding permissible limits by 4–9× — has been documented in tested preparations.[10] The FDA has prohibited A. muscaria in conventional food products and has not accepted GRAS or NDI notifications for muscimol.[5]
Per-preparation dose tiers, timelines, and bioavailability data are in the Dose · by preparation card on this page.
Harm Reduction[edit]
Forms & Identification
A. muscaria preparations sold in commerce — gummies, extracts, dried caps, and vape cartridges — lack standardized testing protocols. No ISO/IEC-accredited laboratory testing program exists specifically for muscimol-containing products. Lab testing matters here more than for most plant preparations because: alkaloid concentrations vary dramatically across specimens and processing methods; commercial labeling accuracy is unverified; and heavy metal contamination (cadmium, lead, vanadium) has been documented at levels exceeding permissible safety limits.
For whole dried mushroom material, professional mycological verification of species identity is essential. A. muscaria is visually distinctive in its classic red-capped form, but yellow- and orange-capped varieties can be confused with A. pantherina (higher alkaloid content) or, more dangerously, with amatoxin-containing species that cause lethal liver failure. If purchasing commercial products, request a Certificate of Analysis (CoA) from a third-party laboratory showing alkaloid content and heavy metal testing.
Guidelines
- Start with dried, heat-processed material only. Fresh mushrooms retain an approximately 9:1 ibotenic acid-to-muscimol ratio and carry substantially higher gastrointestinal toxicity and unpredictability.
- Start low. Begin with the lowest suggested dose for your preparation and wait at least 2 hours before considering any additional consumption. Onset can take up to 90 minutes.
- Test your source. If using commercial products, verify the supplier provides third-party lab testing for alkaloid content and heavy metals. Products without a CoA should be treated as unknown-potency preparations.
- Never combine with alcohol, benzodiazepines, or other sedatives. Muscimol's GABA-A agonism creates a direct mechanistic basis for additive CNS and respiratory depression with any GABAergic substance.
- Do not drive or operate machinery. Motor control impairment, confusion, and perceptual distortion make any activity requiring coordination dangerous.
- Have a sober companion present. The deliriant character of moderate-to-high doses means the user may not be able to recognize an emergency or make sound decisions.
- Stay hydrated. Nausea and sweating are common. Maintain fluid intake throughout.
Set & Setting
The A. muscaria experience is characteristically unpredictable: the biphasic shift from excitation to sedation, the deliriant quality at higher doses, and the potential for confusion and impaired reality testing demand careful environmental planning. Use only in a safe, familiar, private setting with no access to water bodies, heights, or roads. A sober, trusted companion is strongly recommended — particularly because higher-dose experiences may involve amnesia and impaired judgment.
Expectations matter: A. muscaria does not produce the clear-headed insight of serotonergic psychedelics. Anticipate a dreamy, disorienting experience closer to a hypnagogic state. Anxiety is common, especially during the initial excitatory phase.
Aftercare & integration. Residual effects — grogginess, confusion, and perceptual oddities — may persist for 10–24 hours after the primary experience. Plan for a full day of recovery with no obligations. Sleep is often disrupted; allow the body to rest without forcing a schedule.
Hydrate and eat lightly. Nausea may linger; bland foods and electrolyte drinks can help. If significant anxiety or confusion persists beyond 24 hours, contact a healthcare provider.
The dreamlike, often fragmentary quality of the experience may benefit from journaling within 24 hours while recall is freshest. Integration is more challenging than with serotonergic psychedelics because memory of the experience is often partial or distorted.
Recovery & Support
No published clinical data characterize a dependence syndrome or withdrawal protocol specific to A. muscaria or muscimol. However, given muscimol's mechanistic parallels to benzodiazepine pharmacology, individuals using A. muscaria preparations frequently or in escalating amounts should approach cessation with caution.
If regular use has developed, taper gradually rather than stopping abruptly. Monitor for rebound effect anxiety, insomnia, or agitation — symptoms that would be consistent with GABAergic withdrawal, though their occurrence with muscimol has not been clinically documented.
For support with any substance use concern:
- SAMHSA National Helpline: 1-800-662-4357 (US, free, confidential, 24/7)
- Crisis Text Line: Text HOME to 741741 (US)
- Poison Control: 1-800-222-1222 (US) for acute ingestion concerns
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Unresponsiveness or inability to be roused
- Breathing that is slow, shallow, or irregular
- Prolonged seizure activity
- Severe confusion with agitation or self-harm risk
- Vomiting while unconscious or semi-conscious
Immediate steps:
- 1. Call emergency services immediately if the person is unresponsive, seizing, or showing breathing difficulties.
- 2. Place an unconscious but breathing person in the recovery position (on their side) to protect the airway.
- 3. Do not induce vomiting.
- 4. Do not administer atropine — it does not address the central mechanism and is not indicated for A. muscaria poisoning.
- 5. Stay with the person. Monitor breathing continuously until help arrives.
What to tell the dispatcher:
State that the person ingested Amanita muscaria (fly agaric mushroom), the approximate amount and form (dried caps, tea, commercial product), the time of ingestion, and current symptoms. Good Samaritan laws exist in many jurisdictions and provide legal protection for those seeking emergency help.
No reversal agent exists for muscimol or ibotenic acid intoxication. Treatment is supportive.
Legal Status[edit]
A. muscaria, muscimol, and ibotenic acid are not listed under any United Nations drug control treaty — neither the 1961 Single Convention on Narcotic Drugs, the 1971 Convention on Psychotropic Substances, nor the 1988 Convention Against Illicit Traffic. The WHO has not conducted a formal review of muscimol for scheduling purposes. Legal status is therefore determined entirely by domestic legislation in individual jurisdictions, producing a patchwork of regulation that ranges from unrestricted legality to outright prohibition.
| Jurisdiction | Status | Notes |
|---|---|---|
| United States (federal) | Not controlled | A. muscaria, muscimol, and ibotenic acid are not listed under the Controlled Substances Act. In December 2024, the FDA prohibited A. muscaria and its specified constituents in conventional food products. No GRAS or NDI notifications have been accepted for muscimol.[5] |
| Louisiana (US state) | Restricted | Act No. 159 (effective August 8, 2005) prohibits A. muscaria intended for human consumption. Possession for aesthetic or decorative purposes is exempted. Louisiana is the only US state with a confirmed explicit ban.[14] |
| Netherlands | Illegal | Banned since end of 2008. Possession of more than 5 g fresh or more than 0.5 g dried constitutes a criminal offense.[14] |
| Australia | Prohibited | Schedule 9 under the Poisons Standard (prohibited except for approved research).[14] |
| Romania | Illegal | Banned since 2010.[6] |
| United Kingdom | Not controlled (disputed) | Not listed under the Misuse of Drugs Act 1971. Marketing for psychoactive effects may invoke the Psychoactive Substances Act 2016.[14] One secondary source claims UK possession and sale are prohibited,[6] conflicting with other UK-specific legal sources. citation needed |
| Germany | Legal | Not classified as a narcotic under the Betäubungsmittelgesetz. This applies to most EU member states where A. muscaria is not specifically scheduled.[10] |
| Canada | Legal | Not scheduled under the Controlled Drugs and Substances Act. citation needed |
| Russia, Sweden, Ukraine, Thailand, Brazil | Restrictions reported | Various restrictions have been reported but specific legislation has not been verified.[5] citation needed |
No structural analog act provisions apply to muscimol or ibotenic acid at the US federal level. Neither compound is a structural analog of any Schedule I or Schedule II substance under the Federal Analogue Act. The remaining 49 US states and the District of Columbia have no confirmed A. muscaria-specific restrictions, though general consumer protection, food safety, and product liability laws may apply to commercial preparations.
Frequently asked questions
What is Amanita muscaria?
Amanita muscaria is a basidiomycete fungus containing the GABA-A agonist muscimol and its NMDA-active prodrug ibotenic acid. Consumed for millennia in Siberian shamanic traditions, it produces sedative-oneiric states; no controlled clinical trials have been published.
What are dangerous combinations with Amanita muscaria?
The highest-severity documented interactions for Amanita muscaria: Antipsychotics (Dangerous), Benzodiazepines, Barbiturates (Dangerous), Clonidine, Guanfacine (Dangerous), Gabapentin, Pregabalin (Dangerous), GHB, Baclofen (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is Amanita muscaria addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for Amanita muscaria: tolerance builds unknown; cross-tolerance develops with benzodiazepines, barbiturates, gaboxadol (THIP), other GABA-A agonists. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcOkhovat A, Cruces W, Docampo-Palacios ML, Ray KP, Ramirez GA (2023) Psychoactive Isoxazoles, Muscimol, and Isoxazole Derivatives from the Amanita (Agaricomycetes) Species: Review of New Trends in Synthesis, Dosage, and Biological Properties — International Journal of Medicinal Mushrooms doi:10.1615/intjmedmushrooms.2023049458
- [2] ^abNyberg H (1992) Religious use of hallucinogenic fungi: A comparison between Siberian and Mesoamerican cultures — Karstenia doi:10.29203/ka.1992.294
- [3] ^abcMichelot D, Melendez-Howell LM (2003) Amanita muscaria: chemistry, biology, toxicology, and ethnomycology — Mycological Research doi:10.1017/s0953756203007305
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references
- [1] ^abcOkhovat A, Cruces W, Docampo-Palacios ML, Ray KP, Ramirez GA (2023) Psychoactive Isoxazoles, Muscimol, and Isoxazole Derivatives from the Amanita (Agaricomycetes) Species: Review of New Trends in Synthesis, Dosage, and Biological Properties — International Journal of Medicinal Mushrooms doi:10.1615/intjmedmushrooms.2023049458
- [2] ^abNyberg H (1992) Religious use of hallucinogenic fungi: A comparison between Siberian and Mesoamerican cultures — Karstenia doi:10.29203/ka.1992.294
- [3]
- [4]
- [5]
- [6]