Psilocybin Systematic (IUPAC) name [3-(2-dimethylaminoethyl)-1H-indol-4-yl] dihydrogen phosphate Clinical data AHFS/Drugs.com Pregnancy cat. ? Legal status Prohibited (S9) (AU) Schedule III (CA) ? (UK) Schedule I (US) Identifiers CAS number ATC code None PubChem ChemSpider KEGG ChEBI ChEMBL Chemical data Formula C12H17N2O4P Mol. mass 284.25 g/mol SMILES & Physical data Melt. point 190–198 °C (374–388 °F) (what is this?)
Psilocybin ( // sil-ə-sy-bin; alternatively spelled psilocybine) is a naturally occurring psychedelic prodrug, with mind-altering effects similar to those of LSD and mescaline, after it is converted to psilocin. The effects can include altered thinking processes, perceptual distortions, an altered sense of time, and spiritual experiences, as well as adverse reactions such as nausea and panic attacks. Psilocybin is produced by over 200 species of mushrooms. The most potent are members of the genus Psilocybe, such as P. cubensis, P. semilanceata, and P. cyanescens, but psilocybin has also been isolated from about a dozen other genera, collectively known as psilocybin mushrooms.
In Mexico, Central America, and South America, psilocybin-containing mushrooms have been ingested for thousands of years, primarily for spiritual purposes. In a 1957 Life magazine article, American banker and ethnomycologist R. Gordon Wasson described his experiences ingesting psilocybin-containing mushrooms during a traditional ceremony in Mexico, introducing the drug to popular culture. Shortly afterward the Swiss chemist Albert Hofmann was able to purify the active principle psilocybin from the mushroom Psilocybe mexicana, and developed a method to produce the drug synthetically. Hofmann's employer Sandoz marketed and sold pure psilocybin to physicians and clinicians worldwide for use in psychedelic psychotherapy.
Enthusiasts for the drug consider it an entheogen (spirituality-enhancing agent) and a tool to supplement practices for transcendence, including meditation and psychonautics. The intensity and duration of the effects of psilocybin are variable, depending on species or cultivar of mushrooms, dosage, individual physiology, and set and setting, as was shown in experiments led by Timothy Leary at Harvard University in the early 1960s. Once ingested, psilocybin is rapidly metabolized to psilocin, which then acts on serotonin receptors in the brain. The mind-altering effects of psilocybin typically last from two to six hours; however, to individuals under the influence of psilocybin, the effects may seem to last much longer, since the drug can distort the perception of time. Psilocybin has a low toxicity, and reports of lethal doses of the drug are rare. Several modern bioanalytical methods have been adapted to rapidly and accurately screen the levels of psilocybin in mushroom samples and body fluids. Possession of psilocybin-containing mushrooms has been outlawed in most countries, and it has been classified as scheduled by many national drug laws.
- 1 History
- 2 Occurrence
- 3 Chemistry
- 4 Toxicity and harm potential
- 5 Physiology
- 6 Effects
- 7 Mystical experiences
- 8 Use in medicine
- 9 Social and legal aspects
- 10 See also
- 11 Notes
- 12 References
- 13 External links
- 14 Further reading
There is evidence to suggest that psychoactive mushrooms have been used by man in religious ceremonies for thousands of years. Rock art discovered near the town of Villar del Humo in Spain offers evidence that Psilocybe hispanica was used in religious rituals 6000 years ago; similarly, murals dated 7000 to 9000 BCE found in the Sahara desert in southeast Algeria suggest prehistoric usage of psilocybin mushrooms. In the Mayan and Aztec cultures, psilocybin mushrooms were used for rituals and ceremonies; in Nahuatl, the language of the Aztecs, the mushrooms were called teonanacatl, or "God's flesh". Following the arrival of Spanish explorers to the New World in the 16th century, chroniclers reported the use of mushrooms by the natives for ceremonial and religious purposes. According to the Dominican friar Diego Durán in The History of the Indies of New Spain (published circa 1581), mushrooms were eaten in festivities conducted on the occasion of the accession to the throne of Aztec emperor Moctezuma II in 1502. The Franciscan friar Bernardino de Sahagún wrote of witnessing mushroom usage in his Florentine Codex (1545–1590). In the following passage, he described how some merchants would celebrate upon returning from a successful business trip:
Coming at the very first, at the time of feasting, they ate mushrooms when, as they said, it was the hour of the blowing of the flutes. Not yet did they partake of food; they drank only chocolate during the night. And they ate mushrooms with honey. When already the mushrooms were taking effect, there was dancing, there was weeping.... Some saw in a vision that they would die in war. Some saw in a vision that they would be devoured by wild beasts.... Some saw in a vision that they would become rich, wealthy. Some saw in a vision that they would buy slaves, would become slave owners. Some saw in a vision that they would commit adultery [and so] would have their heads bashed in, would be stoned to death.... Some saw in a vision that they would perish in the water. Some saw in a vision that they would pass to tranquillity in death. Some saw in a vision that they would fall from the housetop, tumble to their death ... All such things they saw.... And when [the effects of] the mushroom ceased, they conversed with one another, spoke of what they had seen in the vision."
After the defeat of the Aztecs, the Spanish conquerors forbade traditional religious practices and rituals, including ceremonial mushroom use. For the next four centuries, the Indians of Mesoamerica hid their use of entheogens from their Spanish conquerors.
American banker and amateur ethnomycologist R. Gordon Wasson and his wife Valentina studied the ritual use of psychoactive mushrooms by the native population in the Mazatec village Huautla de Jiménez. In 1957, they published an article in Life magazine (Seeking the Magic Mushroom) in which they described the occurrence of hallucinatory experiences during these rituals. Later the same year they were accompanied on a followup expedition by the French mycologist Roger Heim, who identified several of the mushrooms as Psilocybe species. Heim was able to cultivate the mushrooms in France, and sent samples for analysis to the chemist Albert Hofmann, who was working for the Swiss multinational pharmaceutical company Sandoz (now Novartis). Hofmann, who had in 1938 created LSD, was the first to recognize the importance and chemical structure of the pure compounds he called psilocybin and psilocin. Leading a research group that was able to isolate and identify the compounds from Psilocybe mexicana, Hofmann was aided in the discovery process by his willingness to ingest mushroom extracts. He and his colleagues later synthesized a number of compounds chemically related to the naturally occurring psilocybin:
In essence, these were the same molecules except that: (1) the phosphoryl or hydroxy group at the top of the indole ring was moved around to other ring positions, and (2) different numbers of methyl groups (CH3) and other carbon chains were added to the side-chains and to the nitrogen on the indole ring to see how these changes would affect psychoactivity.
Two diethyl (containing two ethyl groups in place of the two methyl groups) analogs of psilocybin and psilocin were synthesized by Hofmann, 4-phosphoryloxy-N,N-diethyltryptamine, called CEY-19, and 4-hydroxy-N,N-diethyltryptamine, called CZ-74. Because their physiological effects last only about three and a half hours (compared to roughly double that with psilocybin), they proved more manageable in European clinics using "psycholytic therapy"—a form of psychotherapy that advocates the controlled use of psychedelic drugs. Sandoz marketed and sold pure psilocybin under the name Indocybin to physicians and clinicians worldwide. There were no reports of serious complications when psilocybin was used in this way.
In the early 1960s, Harvard University became a testing ground for psilocybin, through the efforts of Timothy Leary and his associate Richard Alpert (who later changed his name to Ram Dass). Leary was able to obtain synthesized psilocybin from Hofmann through Sandoz pharmaceutical. Although some studies in the early 1960s, such as the Concord Prison Experiment, suggested positive results using psilocybin in clinical psychiatry, the backlash against LSD usage swept psilocybin along with it into the Schedule I category of illicit drugs in 1970. In the Unites States, rules were introduced to restrict the use of the drug in human research, and scientists who worked with the drug faced reduced funding and being "professionally marginalized".
Despite the legal restrictions on psilocybin use, the 1970s witnessed the emergence of psilocybin as the "entheogen of choice". This was due in large part to a wide dissemination of information on the topic, which included works such as those by author Carlos Castaneda, and several books that taught the technique of growing psilocybin mushrooms. One of the most popular of these books was produced under the pseudonyms O.T. Oss and O.N. Oeric by Jeremy Bigwood, Dennis J. McKenna, K. Harrison McKenna, and Terence McKenna, entitled Psilocybin: Magic Mushroom Grower's Guide. Over 100,000 copies had been sold by 1981. As ethnologist Jonathan Ott explains, "These authors adapted San Antonio's technique (for producing edible mushrooms by casing mycelial cultures on a rye grain substrate; San Antonio 1971) to the production of Psilocybe [Stropharia] cubensis. The new technique involved the use of ordinary kitchen implements, and for the first time the layperson was able to produce a potent entheogen in his own home, without access to sophisticated technology, equipment or chemical supplies."
Because of a lack of clarity about laws about psilocybin mushrooms, retailers in the late 1990s and early 2000s commercialized and marketed them in smartshops in the Netherlands and the UK, and on the internet. Several websites emerged that have contributed to the accessibility of information on description, use, effects and exchange of experiences among users. Since 2001, six EU countries have tightened their legislation on psilocybin mushrooms in response to concerns regarding their prevalence and increasing usage. In the 2000s, psilocybin and its effects on human consciousness were again the subject of scientific study.
Psilocybin is a naturally occurring compound found in varying concentrations in over 200 species of Basidiomycota mushrooms. In a 2000 review on the worldwide distribution of hallucinogenic mushrooms, Gastón Guzmán and colleagues considered these to be distributed amongst the following genera: Psilocybe (116 species), Gymnopilus (14), Panaeolus (13), Copelandia (12), Hypholoma (6), Pluteus (6) Inocybe (6), Conocybe (4), Panaeolina (4), Gerronema (2) and Agrocybe, Galerina and Mycena (1 species each). Guzmán increased his estimate of the number of psilocybin-containing Psilocybe to 144 species in a 2005 review. Of these, 53 are found in Mexico, 22 in Canada and the US, 16 in Europe, 15 in Asia, 4 in Africa, 19 in Australia and associated islands. In general, psilocybin-containing species are dark-spored, gilled mushrooms that grow in meadows and woods of the subtropics and tropics, usually in soils rich in humus and plant debris. Psilocybin mushrooms occur on all continents, but the majority of species are found in subtropical humid forests. Psilocybe species commonly found in the tropics include P. cubensis and P. subcubensis. P. semilanceata is common in Europe, Canada, and the United States, but is not found in Mexico. Although the presence or absence of psilocybin is not of much use as a chemotaxonomical marker at the familial level or higher, it is used to classify taxa of lower taxonomic groups.
Mushroom caps tend to contain more of the psychoactive compounds than the stems. The spores of these mushrooms do not contain psilocybin or psilocin. The total potency varies greatly between species and even between specimens of one species collected from the same fungus. Because most psilocybin biosynthesis occurs early in the formation of fruit bodies or sclerotia, younger, smaller mushrooms tend to have a higher concentration of the drug than larger, mature mushrooms. In general, the psilocybin content of mushrooms is quite variable (ranging from almost nothing to 1.5% of the dry weight) and depends on species, growth and drying conditions, and mushroom size. The drug is more stable in dried than fresh mushrooms; dried mushrooms retain their potency for months or even years, while mushrooms stored fresh for four weeks contain only traces of the original psilocybin. Mature mycelia contain some psilocybin, while young mycelia (recently germinated from spores) lack appreciable amounts. Many species of mushrooms containing psilocybin also contain small amounts of the analog compounds baeocystin and norbaeocystin, chemicals thought to be biogenic precursors. Most species of psilocybin-containing mushrooms bruise blue when handled or damaged due to the oxidization of phenolic compounds. This reaction, however, is not a definitive method of identification or determining a mushroom's potency.
Psilocybin (O-phosphoryl-4-hydroxy-N,N-dimethyltryptamine or 4-PO-DMT) is a prodrug that is converted into the pharmacologically active compound psilocin in the body by a dephosphorylation reaction. This chemical reaction takes place under strongly acidic conditions, or under physiological conditions in the body, through the action of enzymes called phosphatases. Oxidization of psilocin by the enzyme hydroxyindole oxidase yields the deep blue-colored compound ortho-quinone. This compound readily undergoes electron transfer, a chemical feature that contributes to the biochemical effects of psilocybin.
Psilocybin is a tryptamine compound having a chemical structure derived from the amino acid tryptophan and containing an indole linked to an ethylamine substituent; psilocybin bears a close structural resemblance to the neurotransmitter serotonin (5-hydroxytryptamine). Biosynthetically, the biochemical transformation from tryptophan to psilocybin involves several enzyme reactions: decarboxylation, methylation at the N9 position, 4-hydroxylation, and O-phosphorylation. Isotopic labeling experiments suggest that tryptophan decarboxylation is the first biosynthetic step and that O-phosphorylation is the final step. The precise sequence of the intermediate steps is not known with certainty, and the biosynthetic pathway may differ between species.
Psilocybin is a zwitterionic alkaloid that is soluble in water, moderately soluble in methanol and ethanol, and insoluble in most organic solvents. Exposure to light is detrimental to the stability of aqueous solutions of psilocybin, and will cause it to rapidly oxidize—an important consideration when using it as an analytical standard. Osamu Shirota and colleagues reported a method for the large-scale synthesis of psilocybin without chromatographic purification in 2003. Starting with 4-hydroxyindole, they generated psilocybin from psilocin at an 85% yield, a marked improvement over yields reported from previous syntheses. Purified psilocybin is a white, needle-like crystalline powder with a melting point between 190–198 °C (374–388 °F).
Several relatively simple chemical tests—commercially available as reagent testing kits—can be used to detect the presence of psilocybin in mushroom extracts. The drug reacts in the Marquis test to produce a yellow color, and a green color in the Mandelin test. Ehrlich's reagent and DMACA reagent are used as sprays to detect the drug after thin layer chromatographic analysis. Many modern analytical techniques have been adapted to determine the quantity of psilocybin in mushroom material. The earliest techniques used gas chromatography; however, a problem with this method is that psilocybin dephosphorylates to psilocin prior to analysis, making it difficult to discriminate between the two drugs. In forensic toxicology, techniques involving gas chromatography coupled to mass spectrometry (GC–MS) are the most widely used due to their high sensitivity and ability to separate compounds in complex biological mixtures. These techniques include ion mobility spectrometry, capillary zone electrophoresis, ultraviolet spectroscopy, and infrared spectroscopy. High performance liquid chromatography (HPLC) is used with ultraviolet, fluorescence, electrochemical, and electrospray mass spectrometric detection methods.
Various chromatographic methods have been developed to detect psilocin in body fluids: the rapid emergency drug identification system (REMEDi HS), a drug screening method based on HPLC; HPLC with electrochemical detection; GC–MS; and liquid chromatography coupled to mass spectrometry. Although the determination of psilocin levels in urine can be performed without sample clean-up (i.e., removing potential contaminants that make it difficult to accurately assess concentration), the analysis in plasma or serum requires a preliminary extraction, followed by derivatization of the extracts in the case of GC–MS. A specific immunoassay has also been developed to detect psilocin in whole blood samples. A 2009 publication reported using HPLC to obtain a high-speed separation of forensically important illicit drugs including psilocybin and psilocin, which were identifiable within 0.5 min of analysis. These analytical techniques to determine psilocybin concentrations in body fluids are, however, not routinely available, and not typically used in clinical settings.
Psilocybin is rapidly dephosphorylated in the body to psilocin, which then acts as a partial agonist to several receptors involved with the neurotransmission of serotonin. Psilocin has a high affinity for the 5-HT2A serotonin receptor in the brain, where it mimics the effects of serotonin (5-HT). Psilocin binds less tightly to other serotonergic receptors 5-HT1A, 5-HT1D, and 5-HT2C. Serotonin receptors are located in numerous parts of the brain including the cerebral cortex, and are involved in a wide range of functions, including regulation of mood and motivation. The psychotomimetic effects of psilocin can be blocked in a dose-dependent fashion by the 5-HT2A antagonist drugs ketanserin and risperidone. Although the 5-HT2A receptor is responsible for most of the effects of psilocybin, various lines of evidence have shown that interactions with non-5-HT2A receptors also contribute to the subjective and behavioral effects of the drug.[nb 1]
The chemical structures of psilocybin and related analogs have been used in computational biology to help model the structure, function, and ligand-binding properties of the 5-HT2C G-protein-coupled receptor. In contrast to LSD, psilocybin and psilocin have no affinity for the dopamine D2 receptor.
Toxicity and harm potential
The toxicity of psilocybin is low; in rats, the oral LD50 is 280 mg/kg, approximately one and a half times that of caffeine. When administered intravenously in rabbits, psilocybin's LD50 is approximately 12.5 mg/kg (rabbits, however, are extremely intolerant to the effects of most psychoactive drugs). Based on the results of animal studies, the lethal dose of psilocybin has been extrapolated to be 6 grams. The Registry of Toxic Effects of Chemical Substances gives psilocybin a relatively high therapeutic index of 641 (higher values correspond to a better safety profile); for comparison, the therapeutic indexes of aspirin and nicotine are 199 and 21, respectively. The lethal dose from psilocybin toxicity alone is unknown at recreational or medicinal levels, and has rarely been documented—as of 2011, only two cases attributed to overdosing on hallucinogenic mushrooms (without simultaneous use of other drugs) have been reported in the scientific literature. Psilocybin makes up roughly 1% of the weight of Psilocybe cubensis mushrooms, and so nearly 1.7 kilograms of dried mushrooms, or 17 kilograms of fresh mushrooms, would be required for a 60 kg person to reach the 280 mg/kg LD50 rate of rats. Although experiments with mice have shown no evidence that the drug causes birth defects, it is recommended that pregnant women avoid its usage.
Repeated use of psilocybin does not lead to physical dependence on the drug. A 2008 study concluded that, based on US data from the period 2000–2002, adolescent-onset (defined here as ages 11–17) usage of hallucinogenic drugs (including psilocybin) did not increase the risk of drug dependence in adulthood; this was in contrast to adolescent usage of cannabis, cocaine, inhalants, anxiolytic medicines, and stimulants, all of which were associated with "an excess risk of developing clinical features associated with drug dependence". Similarly, a 2010 Dutch study ranked the relative harm of psilocybin mushrooms compared to a selection of 19 recreational drugs, including alcohol, cannabis, cocaine, ecstasy, heroin, and tobacco. Experts rated the drugs for their acute and chronic toxicity, addictive potency, and social harm. Magic mushrooms were ranked as the illicit drug with the lowest harm, corroborating conclusions reached earlier by expert groups in the United Kingdom.
The effects of the drug begin 10–40 minutes after ingestion of psilocybin-containing mushrooms, and last 2–6 hours depending on dose, species, and individual metabolism. A typical recreational dosage is 10–50 mg psilocybin, although only 4–10 mg (corresponding roughly to 50–300 micrograms per kilogram of body weight) are required to induce hallucinogenic effects. However, a small number of people are unusually sensitive to psilocybin's effects, such that a normally threshold-level dose of around 2 mg of psilocybin can result in effects usually associated with medium or high doses. Conversely, there are some people who require relatively high doses of psilocybin to get noticeable effects. Individual brain chemistry and metabolism play a large role in determining a person's response to psilocybin.
Based on studies using animals, about 50% of ingested psilocybin is absorbed through the stomach and intestine. Within 24 hours, about 65% of the absorbed psilocybin is excreted into the urine, and a further 15–20% is excreted in the bile and feces. Although most of the remaining drug is eliminated in this way within 8 hours, it is still detectable in the urine after 7 days. Psilocybin is metabolized mostly in the liver, where it becomes psilocin, which is broken down by the enzyme monoamine oxidase to produce several metabolites that can circulate in the blood plasma, including 4-hydroxyindole-3-acetaldehyde, 4-hydroxytryptophol, and 4-hydroxyindole-3-acetic acid. Some psilocin is not broken down by enzymes, and instead forms a glucuronide; this is a biochemical mechanism animals use to eliminate toxic substances by linking them with glucuronic acid, which can then be excreted in the urine. Psilocin concentrations in the plasma of adult volunteers averaged about 8 µg/L within 2 hours after ingestion of a single 15 mg oral psilocybin dose; psychological effects occur with a blood plasma concentration of 4–6 µg/L. Psilocybin is about 100 times less potent than LSD on a weight-per-weight basis, and the physiological effects last about half as long.
Tolerance to psilocybin builds and dissipates quickly; ingesting psilocybin more than about once a week can lead to diminished effects. Tolerance dissipates after a few days, so doses can be spaced several days apart to avoid the effect. Studies have demonstrated that a cross-tolerance can develop between psilocybin and the pharmacologically similar LSD; further, cross-tolerance also develops between psilocybin and phenylethylamine hallucinogens such as mescaline and 2,5-dimethoxy-4-methylamphetamine. MAO inhibitors (MAOI) have been known to sustain the effects of psilocybin for longer periods of time; people who are taking an MAOI for a medical condition may experience highly potentiated effects. Acetaldehyde, one of the primary breakdown metabolites of consumed alcohol, reacts with biogenic amines present in the body to produce MAOIs related to tetrahydroisoquinoline and β-carboline, and thus enhance the psychoactive effects of psilocybin. A similar effect has been suggested for tobacco users.
The effects of psilocybin are highly variable and depend on the mindset and environment in which the user has the experience, factors commonly referred to as set and setting. In the early 1960s, Timothy Leary and colleagues at Harvard University investigated the role of set and setting on the effects of psilocybin. They administered the drug to 175 subjects from various backgrounds in a warm, supportive environment free from distractions, intended to be similar to a comfortable living room. Ninety-eight of the subjects were given questionnaires to assess their experiences and the contribution of background and situational factors. Individuals who had experience with psilocybin prior to the study reported more pleasant experiences than those for whom the drug was novel. Group size, dosage, preparation, and expectancy were important determinants of the drug response. Subjects placed in groups of more than eight individuals generally felt that the groups were less supportive, and their experiences were less pleasant. Conversely, smaller groups (fewer than six individuals) were seen as more supportive and subjects reported having more positive reactions to the drug. Leary and colleagues proposed that psilocybin heightens suggestibility, making an individual more receptive to interpersonal interactions and environmental stimuli. These findings were corroborated in a later review by Jos ten Berge (1999), who concluded that dosage, set, and setting were fundamental factors in determining the outcome of experiments that tested the effects of psychedelic drugs on artists' creativity.
After ingesting psilocybin, a wide range of subjective effects may be experienced: feelings of disorientation, lethargy, giddiness, euphoria, joy, and depression. About a third of users report feelings of anxiety or paranoia. At low doses, hallucinatory effects may occur, including enhancement of colors and the animation of geometric shapes. Closed-eye hallucination may occur, in which the affected individual sees multicolored geometric shapes and vivid imaginative sequences. Some individuals report experiencing synesthesia, such as tactile sensations when viewing colors. At higher doses, the altered state of consciousness afforded by psilocybin can lead to "Intensification of affective responses, enhanced ability for introspection, regression to primitive and childlike thinking, and activation of vivid memory traces with pronounced emotional undertones". Open-eye visuals are more common, and may be very detailed although rarely confused with reality.
A 2011 study by Roland R. Griffiths and colleagues suggests that using a single high dosage of psilocybin can cause long-term changes in the personality of its users. Changes in personality were assessed using the Revised NEO Personality Inventory, which describes people's personalities according to five factors: neuroticism, extroversion, conscientiousness, agreeableness, and openness. In the study, about half of the participants—described as healthy, "spiritually active", and many possessing postgraduate degrees—showed an increase in the personality dimension of "openness", and this positive effect was apparent more than a year after the psilocybin session. According to the study authors, the finding is significant because "no study has prospectively demonstrated personality change in healthy adults after an experimentally manipulated discrete event." It is not known whether these results can be generalized to larger populations.
The physical side effects resulting from psilocybin usage are generally not considered significant. Common responses include: pupil dilation (93%); changes in heart rate (100%), including increases (56%), decreases (13%), and variable responses (31%); changes in blood pressure (84%), including hypotension (34%), hypertension (28%), and general instability (22%); changes in stretch reflex (86%), including increases (80%) and decreases (6%); nausea (44%); tremor (25%); and dysmetria (16%) (inability to properly direct or limit motions).[nb 2] The temporary increases in blood pressure caused by the drug can be a risk factor for users with pre-existing hypertension. These qualitative somatic effects caused by psilocybin have been corroborated by several early clinical studies. A 2005 magazine survey of club goers in the UK found that nausea or vomiting was experienced by over a quarter of those who had used hallucinogenic mushrooms in the last year, although this effect is caused by the mushroom rather than psilocybin itself. In one study, administration of gradually-increasing dosages of psilocybin daily for 21 days had no measurable effect on electrolyte levels, blood sugar levels, or liver toxicity tests.
Psilocybin is known to strongly influence the subjective experience of the passage of time. Users often feel as if time is slowed down, resulting in the perception that "minutes appear to be hours" or "time is standing still". These effects can be tested experimentally with timing tasks, in which subjects are tested on their ability to accurately reproduce time intervals of different durations, or to synchronize movements to a sequence of regularly repeated tones. Studies have demonstrated that psilocybin significantly impairs subjects’ ability to gauge time intervals longer than 2.5 seconds, impairs their ability to synchronize to inter-beat intervals longer than 2 seconds, and reduces their preferred tapping rate. These results are consistent with the drug's role in affecting prefrontal cortex activity, and the role that the prefrontal cortex is known to play in time perception.
Users having a pleasant experience can feel an ecstatic sense of connection to others, nature, and the universe; other perceptions and emotions are also often intensified. Users having an unpleasant experience (a "bad trip") describe a reaction accompanied by fear, other unpleasant feelings, and occasionally by dangerous behavior. In general, "bad trip" is used to describe a reaction that is characterized primarily by fear or other unpleasant emotions, not just transitory experience of such feelings. A variety of factors may contribute to a psilocybin user experiencing a bad trip, including "tripping" during an emotional or physical low or in a non-supportive environment (see: set and setting). Ingesting psilocybin in combination with other drugs or with alcohol can also increase the likelihood of a bad trip. Other than the duration of the experience, the effects of psilocybin are similar to comparable dosages of LSD or mescaline. In the Psychedelics Encyclopedia, author Peter Stafford noted "The psilocybin experience seems to be warmer, not as forceful and less isolating. It tends to build connections between people, who are generally much more in communication than when they use LSD."
Possible adverse psychiatric effects
Panic reactions can occur after consumption of psilocybin-containing mushrooms, especially if the ingestion is accidental or otherwise unexpected. Reactions characterized by violence, aggression, homicidal and suicidal attempts, prolonged schizophrenia-like psychosis, and convulsions have been reported in the literature. A 2005 survey of users in the United Kingdom found that almost a quarter of those who had used the drug in the past year had experienced a panic attack. Other adverse effects less frequently reported include paranoia, confusion, derealization, disconnection from reality, and mania. Consumption of psilocybin by those with schizophrenia can induce acute psychotic states requiring hospitalization.
The similarity of psilocybin-induced symptoms to those of schizophrenia has led to the drug being used in both behavioral and neuroimaging studies of this psychotic disorder. In both cases, psychotic symptoms are thought to arise from a "deficient gating of sensory and cognitive information" in the brain that ultimately lead to "cognitive fragmentation and psychosis". There has been one case report of psilocybin and cannabis possibly causing hallucinogen persisting perception disorder (HPPD) (which at worst can last five years or more). However, the claimed association between HPPD and psychedelics is obscured by polydrug use and other variables.
Psychedelic drugs can induce states of consciousness that have lasting personal meaning and spiritual significance in individuals who are religious or spiritually inclined; these states are called mystical experiences. Some scholars have proposed that many of the qualities of a drug-induced mystical experience are indistinguishable from mystical experiences achieved through non-drug techniques, such as meditation or holotropic breathwork. In the 1960s, Walter Pahnke and colleagues sought to more systematically evaluate mystical experiences (which they called "mystical consciousness") by categorizing their common features. These categories, according to Pahnke, "describe the core of a universal psychological experience, free from culturally determined philosophical or theological interpretations", and allow researchers to assess mystical experiences on a qualitative, numerical scale.
In the Marsh Chapel Experiment, which was run by Pahnke at the Harvard Divinity School under the supervision of Timothy Leary, almost all of the graduate degree divinity student volunteers who received psilocybin reported profound religious experiences. One of the participants was religious scholar Huston Smith, author of several textbooks on comparative religion; he later described his experience as "the most powerful cosmic homecoming I have ever experienced." In a 25-year followup to the experiment, all of the subjects given psilocybin described their experience as having elements of "a genuine mystical nature and characterized it as one of the high points of their spiritual life". Psychedelic researcher Rick Doblin considered the study partially flawed due to incorrect implementation of the double-blind procedure, and several imprecise questions in the mystical experience questionnaire. Nevertheless, he said that the study cast "a considerable doubt on the assertion that mystical experiences catalyzed by drugs are in any way inferior to non-drug mystical experiences in both their immediate content and long-term effects". This sentiment was echoed by psychiatrist William A. Richards, who in a 2007 review stated "[psychedelic] mushroom use may constitute one technology for evoking revelatory experiences that are similar, if not identical, to those that occur through so-called spontaneous alterations of brain chemistry."
A group of researchers from Johns Hopkins School of Medicine led by Griffiths conducted a study to assess the immediate and long-term psychological effects of the psilocybin experience, using a modified version of the mystical experience questionnaire and a rigorous double-blind procedure. When asked in an interview about the similarity of his work with Leary's, Griffiths explained the difference: "We are conducting rigorous, systematic research with psilocybin under carefully monitored conditions, a route which Dr. Leary abandoned in the early 1960s." The study, published in 2006, has been praised by experts for the soundness of its experimental design.[nb 3] In the experiment, 36 volunteers without prior experience with hallucinogens were given psilocybin and methylphenidate (Ritalin) in separate sessions; the methylphenidate sessions served as a control and psychoactive placebo. The degree of mystical experience was measured using a questionnaire on mystical experience developed by Ralph W. Hood; 61% of subjects reported a "complete mystical experience" after their psilocybin session, while only 13% reported such an outcome after their experience with methylphenidate. Two months after taking psilocybin, 79% of the participants reported moderately to greatly increased life satisfaction and sense of well-being. About 36% of participants also had a strong to extreme “experience of fear” or dysphoria (i.e., a “bad trip”) at some point during the psilocybin session (which was not reported by any subject during the methylphenidate session), with about one-third of these (13% of the total) reporting that this dysphoria dominated the entire session. These negative effects were reported to be easily managed by the researchers and did not have a lasting negative effect on the subject’s sense of well-being.
A followup study conducted 14 months after the original psilocybin session confirmed that participants continued to attribute deep personal meaning to the experience. Almost one-third of the subjects reported that the experience was the single most meaningful or spiritually significant event of their lives, and over two-thirds reported it among their five most spiritually significant events. About two-thirds indicated that the experience increased their sense of well-being or life satisfaction. Similarly, in a recent (2010) web-based questionnaire study designed to investigate user perceptions of the benefits and harms of hallucinogenic drug use, 60% of the 503 psilocybin users reported that their use of psilocybin had a long-term positive impact on their sense of well-being.
In 2011, Griffiths and colleagues published the results of further studies designed to learn more about the optimum psilocybin doses needed for positive life-changing experiences, while minimizing the chance of negative reactions. In a 14 month followup, the researchers found that 94% of the volunteers rated their experiences with the drug as one of the top 5 most spiritually significant of their lives (44% said it was the single most significant). None of the 90 sessions that took place throughout the study were rated as decreasing well-being or life satisfaction. Moreover, 89% reported positive changes in their behaviors as a result of the experiences. The conditions of the experimental design included a single drug experience a month, on a couch, in a living-room-like setting, with eye shades and carefully chosen music (classical and world music). As an additional precaution to guide the experience, the 2011 study included a "monitor" whom the volunteers supposedly trusted. The monitors provided gentle reassurance when the volunteers experienced times of anxiety. The volunteers, monitors, and observers all remained blind to the exact dosages for the sake of the experiment.
Use in medicine
Psilocybin has been investigated as an experimental treatment for several disorders. In 1961, Timothy Leary and Richard Alpert ran the Harvard Psilocybin Project, carrying out a number of experiments concerning the use of psilocybin in the treatment of personality disorders and other uses in psychological counseling. In the late 1960s, in response to concerns about the increase in unauthorized use of psychedelic drugs by the general public, psilocybin and other hallucinogenic drugs suffered negative press and faced increasingly restrictive laws. Human research relating to the therapeutic applications of psychedelic drugs was subsequently curbed, and funding for such projects became difficult to obtain. In the 2000s, there has been a resurgence of research concerning the use of psychedelic drugs to explore the nature of the mystical experience, or for clinical applications, such as to address anxiety disorders, major depression, and various addictions.
A pilot study led by Francisco Moreno at the University of Arizona and supported by the Multidisciplinary Association for Psychedelic Studies studied the effects of psilocybin on nine patients with obsessive-compulsive disorder (OCD). The study found that in a controlled clinical environment, the use of psilocybin was associated with substantial reductions in OCD symptoms in several of the patients. This effect may be caused by psilocybin's ability to reduce the levels of the serotonin-2A receptor, resulting in decreased responsiveness to serotonin. In addition, psilocybin has shown promise to ease the pain caused by cluster headaches, often considered not only the most painful of all types of headaches but "one of the worst pain syndromes known to mankind." In a 2006 study, most cluster headache patients who used psilocybin reported that the drug successfully aborted the attacks and extended the length of the remission period. Despite flaws in the study design, the results suggest that psilocybin merits further study for use in the prevention of cluster headaches—only subhallucinogenic doses of the drug are required for effective treatment, and no other medication has been reported to stop a cluster headache cycle.
Two current studies have investigated the possibility that psilocybin can ease the psychological suffering associated with cancer. One study, led by Charles Grob, involved 12 subjects with terminal cancer being administered the hallucinogen or a placebo in two separate sessions. A second study, led by Roland Griffiths at Johns Hopkins, administered psilocybin to people "with a current or past diagnosis of cancer who have some anxiety or are feeling down about their cancer". Preliminary results indicate that low doses of psilocybin can improve the mood and reduce anxiety of patients with advanced cancer, and that the effects last from two weeks to six months. In 2008, the Johns Hopkins research team published guidelines for responsibly conducting medical research trials with psilocybin and other hallucinogens in humans. These included recommendations on how to screen potential study volunteers to exclude those with personal or family psychiatric histories suggesting risk of averse reactions to hallucinogens.
Social and legal aspects
In the United States, psilocybin (and psilocin) were first subjected to federal regulation by the Drug Abuse Control Amendments of 1965, a product of a bill sponsored by Senator Thomas J. Dodd. The law—passed in July 1965 and taking effect on February 1, 1966—was an amendment to the federal Food, Drug and Cosmetic Act and was intended to regulate the unlicensed "possession, manufacture, or sale of depressant, stimulant and hallucinogenic drugs". The statutes themselves, however, did not list the "hallucinogenic drugs" that were being regulated. Instead the term "hallucinogenic drugs" was meant to refer to those substances believed to have a "hallucinogenic effect on the central nervous system".
Despite the seemingly strict provisions of the law, many people were exempt from prosecution. The statutes "permit[ted] … people to possess such drugs so long as they were for the personal use of the possessor, [for] a member of his household, or for administration to an animal". The federal law that specifically banned psilocybin and psilocin was enacted on October 24, 1968. The latter substances were said to have "a high potential for abuse", "no currently accepted medical use," and "a lack of accepted safety". On October 27, 1970, both psilocybin and psilocin became classified as Schedule I and were simultaneously labeled "hallucinogens" under a section of the "Comprehensive Drug Abuse Prevention and Control Act" known as the "Controlled Substances Act". Schedule I drugs are illicit drugs that are claimed to have no known therapeutic benefit. Parties to the treaty are required to restrict use of the drug to medical and scientific research under strictly controlled conditions. Most national drug laws have been amended to reflect this convention (for example, the US Psychotropic Substances Act, the UK Misuse of Drugs Act 1971, and the Canadian Controlled Drugs and Substances Act), with possession and use of psilocybin and psilocin being prohibited under almost all circumstances, and often carrying severe legal penalties.
Possession and use of psilocybin mushrooms, including the bluing species of Psilocybe, is therefore prohibited by extension. However, in many national, state, and provincial drug laws, there is a great deal of ambiguity about the legal status of psilocybin mushrooms and the spores of these mushrooms, as well as a strong element of selective enforcement in some places. In addition, there has been a general shift in attitudes regarding research with psilocybin and other hallucingenic agents; after a long interruption in the use of these drugs, many countries are revising their positions and have started to approve studies to test the physiological and therapeutic effects of hallucinogens.
- ^ Subjective effects are "feelings, perceptions, and moods personally experienced by an individual"; they are often assessed using methods of self-report, including questionnaires. Behavioral effects, in contrast, can be observed directly.
- ^ Percentages are derived from a non-blind clinical study of 30 individuals who were given a dosage of 8–12 milligrams of psilocybin; from Passie (2002), citing Quentin (1960).
- ^ The academic communities' approval for the methodology employed is exemplified by the quartet of commentaries published in the journal Psychopharmacology titled "Commentary on: Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual experience by Griffiths et al.", by HD Kleber (pp. 291–2), DE Nichols (pp. 284–6), CR Schuster (pp. 289–90), and SH Snyder (pp. 287–8).
- ^ Pagliaro LA, Pagliaro AM. (2004). Pagliaro's Comprehensive Guide to Drugs and Substances of Abuse. Washington, D.C.: American Pharmacists Association. p. 324. ISBN 9781582120669.
- ^ Akers BP, Ruiz JF, Piper A, Ruck CA. (2011). "A prehistoric mural in Spain depicting neurotropic Psilocybe mushrooms?". Economic Botany 65 (2): 121–8. doi:10.1007/s12231-011-9152-5.
- ^ Samorini G. (1992). "The oldest representations of hallucinogenic mushrooms in the world (Sahara Desert, 9000–7000 B.P.)". Integration 2 (3): 69–78. http://www.artepreistorica.com/2009/12/the-oldest-representations-of-hallucinogenic-mushrooms-in-the-world-sahara-desert-9000-%E2%80%93-7000-b-p/.
- ^ Marley (2010), p. 164.
- ^ Hofmann A. (1980). "The Mexican relatives of LSD". LSD: My Problem Child. New York, New York: McGraw-Hill. ISBN 9780070293250.
- ^ Marley (2010), p. 165.
- ^ Wasson RG. (13 May 1957). "Seeking the magic mushroom". Life (Time Inc.): 101–20. ISSN 00243019. http://books.google.com/books?id=Jj8EAAAAMBAJ&pg=PA101.
- ^ Heim R. (1957). "Notes préliminaires sur les agarics hallucinogènes du Mexique [Preliminary notes on the hallucination-producing agarics of Mexico]" (in French). Revue de Mycologie 22 (1): 58–79.
- ^ Hofmann A, Heim R, Brack A, Kobel H. (1958). "Psilocybin, ein psychotroper Wirkstoff aus dem mexikanischen Rauschpilz Psilocybe mexicana Heim [Psilocybin, a psychotropic drug from the Mexican magic mushroom Psilocybe mexicana Heim]" (in German). Experientia 14 (3): 107–9. doi:10.1007/BF02159243. PMID 13537892.
- ^ Hofmann A, Heim R, Brack A, Kobel H, Frey A, Ott H, Petrzilka T, Troxler F. (1959). "Psilocybin und Psilocin, zwei psychotrope Wirkstoffe aus mexikanischen Rauschpilzen [Psilocybin and psilocin, two psychotropic substances in Mexican magic mushrooms]" (in German). Helvetica Chimica Acta 42 (5): 1557–72. doi:10.1002/hlca.19590420518.
- ^ Fusar-Poli P, Borgwardt S. (2008). "Albert Hofmann, the father of LSD (1906–2008)" (PDF). Neuropsychobiology 58 (1): 53–4. doi:10.1159/000157779. PMID 18799895. http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=157779&Ausgabe=240319&ProduktNr=224082&filename=157779.pdf.
- ^ a b Stafford (1992), p. 237.
- ^ Marley (2010), p. 166.
- ^ a b c d e f g h Passie T, Seifert J, Schneider U, Emrich HM. (2002). "The pharmacology of psilocybin". Addiction Biology 7 (4): 357–64. doi:10.1080/1355621021000005937. PMID 14578010.
- ^ a b Leary T, Litwin GH, Metzner R. (1963). "Reactions to psilocybin administered in a supportive environment". Journal of Nervous and Mental Disease 137 (6): 561–73. doi:10.1097/00005053-196312000-00007. PMID 14087676.
- ^ Leary T, Metzner R, Presnell M, Weil G, Schwitzgebel R, Kinne S. (1965). "A new behavior change program using psilocybin". Psychotherapy: Theory, Research & Practice 2 (2): 61–72. doi:10.1037/h0088612.
- ^ Griffiths RR, Grob CS. (2010). "Hallucinogens as medicine" (PDF). Scientific American 303 (6): 77–7. doi:10.1038/scientificamerican1210-76. http://www.csp.org/psilocybin/SciAmHallucinogens201012.pdf.
- ^ Ott (1993), p. 276.
- ^ Oeric OT, Os ON. (1991). Psilocybin: Magic Mushroom Grower's Guide (2nd ed.). San Francisco, California: Quick American Archives. ISBN 9780932551061.
- ^ Ott (1993), p. 290. San Antonio's technique describes a method to grow the common edible mushroom Agaricus bisporus; see San Antonio JP. (1971). "A laboratory method to obtain fruit from cased grain spawn of the cultivated mushroom, Agaricus bisporus". Mycologia 63 (1): 16–21. doi:10.2307/3757680. JSTOR 3757680. PMID 5102274. http://www.cybertruffle.org.uk/cyberliber/59350/0063/001/0016.htm.
- ^ Hillebrand J, Olszewski D, Sedefov R. (2006) (PDF). Hallucinogenic Mushrooms: An Emerging Trend Case Study (Report). Lisbon, Portugal: European Monitoring Centre for Drugs and Drug Addiction (EMCDDA). ISBN 9291682497. http://www.emcdda.europa.eu/attachements.cfm/att_31215_EN_TP_Hallucinogenic_mushroom.pdf.
- ^ Keim B. (1 July, 2008). "Psilocybin study hints at rebirth of hallucinogen research". Wired.com. http://www.wired.com/wiredscience/2008/07/psilocybin-stud/. Retrieved 2011-08-08.
- ^ Miller G. (1 July, 2008). "A very memorable trip". ScienceNow. http://news.sciencemag.org/sciencenow/2008/07/01-01.html. Retrieved 2011-08-08.
- ^ a b Guzmán G, Allen JW, Gartz J. (2000). "A worldwide geographical distribution of the neurotropic fungi, an analysis and discussion" (PDF). Annali del Museo Civico di Rovereto: Sezione Archeologia, Storia, Scienze Naturali 14: 189–280. http://www.museocivico.rovereto.tn.it/UploadDocs/104_art09-Guzman%20&%20C.pdf.
- ^ a b Guzmán G. (2005). "Species diversity of the genus Psilocybe (Basidiomycotina, Agaricales, Strophariaceae) in the world mycobiota, with special attention to hallucinogenic properties". International Journal of Medicinal Mushrooms 7 (1–2): 305–31. doi:10.1615/IntJMedMushr.v7.i12.
- ^ Wurst et al. (2002), p. 5.
- ^ Saupe SG. (1981). "Occurrence of psilocybin/psilocin in Pluteus salicinus (Plutaceae)". Mycologia 73 (4): 871–4. JSTOR 3759505. http://www.cybertruffle.org.uk/cyberliber/59350/0073/004/0781.htm.
- ^ Wurst MM, Semerdzieva M, Vokoun J. (1984). "Analysis of psychotropic compounds in fungi of the genus Psilocybe by reversed-phase high performance liquid chromatography". Journal of Chromatography 286: 229–35. doi:10.1016/S0021-9673(01)99190-3.
- ^ Kysilka R, Wurst M. (1989). "High-performance liquid chromatographic determination of some psychotropic indole derivatives". Journal of Chromatography 464 (2): 434–7. PMID 2722990.
- ^ a b Keller T, Schneider A, Regenscheit P, Dirnhofer R, Rücker T, Jaspers J, Kisser W. (1999). "Analysis of psilocybin and psilocin in Psilocybe subcubensis Guzmán by ion mobility spectrometry and gas chromatography-mass spectrometry". Forensic Science International 99 (2): 93–105. doi:10.1016/S0379-0738(98)00168-6. PMID 10077856.
- ^ a b Bigwood J, Beug MW. (1982). "Variation of psilocybin and psilocin levels with repeated flushes (harvests) of mature sporocarps of Psilocybe cubensis (Earle) Singer". Journal of Ethnopharmacology 5 (3): 287–91. doi:10.1016/0378-8741(82)90014-9. PMID 7201054.
- ^ Gartz J. (1992). "New aspects of the occurrence, chemistry and cultivation of European hallucinogenic mushrooms". Supplemento agli Annali dei Musei Civici di Rovereto Sezione Archeologica, Storia e Scienze Naturali 8: 107–24.
- ^ Stafford (1992), p. 248.
- ^ Borowiak KS, Ciechanowski K, Waloszczyk P. (1998). "Psilocybin mushroom (Psilocybe semilanceata) intoxication with myocardial infarction". Journal of Toxicology – Clinical Toxicology 36 (1–2): 47–9. doi:10.3109/15563659809162584. PMID 9541042.
- ^ Stamets (1996), pp. 51–2.
- ^ a b c d e f g h i j k van Amsterdam J, Opperhuizen A, van den Brink W. (2011). "Harm potential of magic mushroom use: a review". Regulatory Toxicology and Pharmacology 59 (3): 423–9. doi:10.1016/j.yrtph.2011.01.006. PMID 21256914.
- ^ Gross ST. (2000). "Detecting psychoactive drugs in the developmental stages of mushrooms". Journal of Forensic Sciences 45 (3): 527–37. PMID 10855955.
- ^ Gartz J. (1987). "Occurrence of psilocybin and baeocystin in fruit bodies of Pluteus salicinus". Planta Medica 53 (3): 290–1. doi:10.1055/s-2006-962710. PMID 17269025.
- ^ Stijve T, Kuyper TW. (1985). "Occurrence of psilocybin in various higher fungi from several European countries". Planta Medica 51 (5): 385–7. doi:10.1055/s-2007-969526. PMID 17342589.
- ^ Repke DB, Leslie DT, Guzmán G. (1977). "Baeocystin in Psilocybe, Conocybe and Panaeolus". Lloydia 40 (6): 566–78. PMID 600026.
- ^ Ballesteros et al. (2006), p. 170.
- ^ Singer R, Smith AH. (1958). "Mycological investigations on Teonanácatl, the Mexican hallucinogenic mushroom. Part II. A taxonomic monograph of Psilocybe, section Caerulescentes". Mycologia 50 (2): 262–303. doi:10.2307/3756197. http://www.cybertruffle.org.uk/cyberliber/59350/0050/002/0262.htm.
- ^ Stamets (1996), pp. 56–8.
- ^ Horita A, Weber LJ. (1961). "Dephosphorylation of psilocybin to psilocin by alkaline phosphatase". Proceedings of the Society for Experimental Biology 106 (1): 32–3. PMID 13715851.
- ^ Blaschko H, Levine WG. (1960). "A comparative study of hydroxyindole oxidases". British Journal of Pharmacology 15 (4): 625–33. PMC 1482277. PMID 19108143. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1482277.
- ^ Blaschko H, Levine WG. (1960). "Enzymic oxidation of psilocine and other hydroxyindoles". Biochemical Pharmacology 3 (2): 168–9. doi:10.1016/0006-2952(60)90036-8.
- ^ Kovacic P, Cooksy AL. (2005). "Unifying mechanism for toxicity and addiction by abused drugs: electron transfer and reactive oxygen species". Medical Hypotheses 64 (2): 357–66. doi:10.1016/j.mehy.2004.07.021. PMID 15607571.
- ^ Kovacic P. (2009). "Unifying electron transfer mechanism for psilocybin and psilocin". Medical Hypotheses 73 (4): 626. doi:10.1016/j.mehy.2009.06.022. PMID 19604649.
- ^ Agurell S, Nilsson JL. (1968). "Biosynthesis of psilocybin. Part II. Incorporation of labelled tryptamine derivatives". Acta Chemica Scandinavica 22 (4): 1210–8. PMID 5750023.
- ^ Chilton WS, Bigwood J, Jensen RE. (1979). "Psilocin, bufotenine and serotonin: historical and biosynthetic observations". Journal of Psychedelic Drugs 11 (1–2): 61–9. PMID 392119.
- ^ Wurst et al. (2002), pp. 12–13.
- ^ a b Anastos N, Barnett NW, Pfeffer FM. (2006). "Investigation into the temporal stability of aqueous standard solutions of psilocin and psilocybin using high performance liquid chromatography". Science & Justice 46 (2): 91–6. doi:10.1016/S1355-0306(06)71579-9.
- ^ a b Shirota O, Hakamata W, Goda Y. (2003). "Concise large-scale synthesis of psilocin and psilocybin, principal hallucinogenic constituents of "magic mushroom"". Journal of Natural Products 66 (6): 885–7. doi:10.1021/np030059u. PMID 12828485.
- ^ Troxler F, Seeman F, Hofmann A. (1959). "Abwandlungsprodukte von Psilocybin und Psilocin. 2. Mitteilung über synthetische Indolverbindungen [Modified products of psilocybin and psilocin. 2. Report on synthetic indole compounds]" (in German). Helvetica Chimica Acta 42 (6): 2073–103. doi:10.1002/hlca.19590420638.
- ^ Hofmann A, Frey A, Ott H, Petrzilka T, Troxler F. (1958). "Konstitutionsaufklärung und Synthese von Psilocybin [The composition and synthesis of psilocybin]" (in German). Cellular and Molecular Life Sciences 14 (11): 397–9. doi:10.1007/BF02160424.
- ^ Nichols DE, Frescas S. (1999). "Improvements to the synthesis of psilocybin and a facile method for preparing the o-acetyl prodrug of psilocin". Synthesis 6 (6): 935–8. doi:10.1055/s-1999-3490.
- ^ Jenkins AJ. (2003). "Hallucinogens". In Levine B. Principles of Forensic Toxicology (2nd ed.). Washington, DC: American Association for Clinical Chemistry Press. p. 281. ISBN 9781890883874. http://books.google.com/books?id=k7BInEQ-iqgC&pg=PA281.
- ^ Bresinsky A, Besl H. (1989). A Colour Atlas of Poisonous Fungi: A Handbook for Pharmacists, Doctors, and Biologists. London, UK: Manson Publishing Ltd. p. 113. ISBN 0723415765. http://books.google.com/books?id=EIcQGsZ2kksC&pg=PA113.
- ^ Kamata T, Katagi M, Tsuchihashi H. (2010). "Metabolism and toxicological analyses of hallucinogenic tryptamine analogues being abused in Japan". Forensic Toxicology 28 (1): 1–8. doi:10.1007/s11419-009-0087-9.
- ^ Pedersen-Bjergaard S, Sannes E, Rasmussen K, Tonneson F. (1997). "Determination of psilocybin in Psilocybe semilanceata by capillary zone electrophoresis". Journal of Chromatography 694 (2): 375–81. doi:10.1016/S0378-4347(97)00127-8. PMID 9252052.
- ^ Lee RE. (1985). "A technique for the rapid isolation and identification of psilocin from psilocin/psilocybin-containing mushrooms". Journal of Forensic Science 30 (3): 931–41. doi:10.1520/JFS11028J.
- ^ Wurst M, Kysilka R, Koza T. (1992). "Analysis and isolation of indole alkaloids of fungi by high-performance liquid chromatography". Journal of Chromatography 593 (1–2): 201–8. doi:10.1016/0021-9673(92)80287-5.
- ^ Saito K, Toyo'oka T, Fukushima T, Kato M, Shirota O, Goda Y. (2004). "Determination of psilocin in magic mushrooms and rat plasma by liquid chromatography with fluorimetry and electrospray ionization mass spectrometry". Analytica Chimica Acta 527 (2): 149–56. doi:10.1016/j.aca.2004.08.071.
- ^ a b Lindenblatt H, Kramer E, Holzmann-Erens, Gouzoulis-Mayfrank E, Kovar K. (1998). "Quantitation of psilocin in human plasma by high performance liquid chromatography and electrochemical detection: comparison of liquid-liquid extraction with automated on-line solid-phase extraction". Journal of Chromatography 709 (2): 255–63. doi:10.1016/S0378-4347(98)00067-X. PMID 9657222.
- ^ Rodriguez-Cruz SE. (2005). "Analysis and characterization of psilocybin and psilocin using liquid chromatography-electrospray ionization mass spectrometry (LC-ESI-MS) with collision-induced-dissociation (CID) and source-induced dissociation (SID)". Microgram Journal 3 (3–4): 175–82. http://www.justice.gov/dea/programs/forensicsci/microgram/journal_v3_num34/journal_v3_num34_pg8.html.
- ^ a b Sticht G, Käferstein H. (2000). "Detection of psilocin in body fluids". Forensic Science International 113 (1): 403–7. doi:10.1016/S0379-0738(00)00213-9. PMID 10978655. http://linkinghub.elsevier.com/retrieve/pii/S0379073800002139.
- ^ Kysilka R. (1990). "Determination of psilocin in rat urine by high-performance liquid chromatography with electrochemical detection". Journal of Chromatography 534: 287–90. doi:10.1016/S0378-4347(00)82176-3. PMID 2094720.
- ^ a b Grieshaber AF, Moore KA, Levine B. (2001). "The detection of psilocin in human urine". Journal of Forensic Sciences 46 (3): 627–30. PMID 11373000.
- ^ Kamata T, Nishikawa M, Katagi M, Tsuchihashi H. (2003). "Optimized glucuronide hydrolysis for the detection of psilocin in human urine samples". Journal of Chromatography B 792 (2): 421–7. doi:10.1016/j.jchromb.2003.08.030.
- ^ Albers C, Köhler H, Lehr M, Brinkmann B, Beike J. (2004). "Development of a psilocin immunoassay for serum and blood samples". International Journal of Legal Medicine 118 (6): 326–31. doi:10.1007/s00414-004-0469-9. ISBN 0041400404699. PMID 15526212.
- ^ Lurie I, Li L. (2009). "Use of high-temperature liquid chromatography with sub-2 µm particle C18 columns for the analysis of seized drugs". Journal of Liquid Chromatography & Related Technologies 32 (17–20): 2615–26. doi:10.1080/10826070903245516.
- ^ a b Attema-de Jonge ME, Portier CB, Franssen EJF. (2007). "Automutilatie na gebruik van hallucinogene paddenstoelen [Automutilation after consumption of hallucinogenic mushrooms]" (in Dutch). Nederlands Tijdschrift voor Geneeskunde 151 (52): 2869–72. PMID 18257429.
- ^ Adams JD Jr. (2009). "Chemical interactions with pyramidal neurons in layer 5 of the cerebral cortex: control of pain and anxiety". Current Medicinal Chemistry 16 (27): 3476–9. doi:10.2174/092986709789057626. PMID 19799545.
- ^ a b Vollenweider FX, Vollenweider-Scherpenhuyzen MF, Babler A, Vogel H, Hell D. (1998). "Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action". NeuroReport 9 (17): 3897–902. doi:10.1097/00001756-199812010-00024. PMID 9875725.
- ^ a b Halberstadt AL, Geyer MA. (2011). "Multiple receptors contribute to the behavioral effects of indoleamine hallucinogens". Neuropharmacology 61 (3): 364–81. doi:10.1016/j.neuropharm.2011.01.017. PMC 3110631. PMID 21256140. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3110631.
- ^ Karch SB. (2007). Pharmacokinetics and Pharmacodynamics of Abused Drugs. Boca Raton, Florida: CRC Press. p. 148. ISBN 9781420054583. http://books.google.com/books?id=9fwUQvF4r-cC&pg=PA148.
- ^ Bray JK, Goddard III WA. (2008). "The structure of human serotonin 2c G-protein coupled receptor bound to agonists and antagonists". Journal of Molecular Graphics and Modelling 27 (1): 66–81. doi:10.1016/j.jmgm.2008.02.006. PMID 18499489.
- ^ González-Maeso J, Sealfon SC. (2009). "Agonist-trafficking and hallucinogens". Current Medicinal Chemistry 16 (8): 1017–27. doi:10.2174/092986709787581851. PMID 19275609.
- ^ Fish JM. (2006). Drugs and Society: U.S. Public Policy. Lanham, Maryland: Rowman & Littlefield. pp. 149–62. ISBN 0742542459. http://www.amazon.com/Drugs-Society-U-S-Public-Policy/dp/0742542459.
- ^ "Drug Toxicity". Web.cgu.edu. http://web.cgu.edu/faculty/gabler/drug_toxicity.htm. Retrieved 2011-08-28.
- ^ "Psilocybine: Animal Toxicity Studies". TOXNET—Toxicology Data Network. United States National Library of Medicine, National Institutes of Health. http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~5CqOWu:1. Retrieved 2011-03-05.
- ^ Gable RS. (2004). "Comparison of acute lethal toxicity of commonly abused psychoactive substances" (PDF). Addiction 99 (6): 686–96. doi:0.1111/j.1360-0443.2004.00744.x. PMID 15139867. http://web.cgu.edu/faculty/gabler/toxicity%20Addiction%20offprint.pdf.
- ^ Strassman R, Wojtowicz S, Luna LE, Frecska E. (2008). Inner Paths to Outer Space: Journeys to Alien Worlds through Psychedelics and Other Spiritual Technologies. Rochester, Vermont: Park Street Press. p. 147. ISBN 9781594772245. http://books.google.com/books?id=0P3_kfFtgicC&pg=PT164.
- ^ Miller RM. (2002). Encyclopedia of Addictive Drugs. Westport, Connecticut: Greenwood Publishing Group. p. 395. ISBN 9780313318078. http://books.google.com/books?id=G7As-qawdzMC&pg=PA395.
- ^ Schaefer C. (2001). Drugs During Pregnancy and Lactation: Handbook of Prescription Drugs and Comparative Risk Assessment. Amsterdam, The Netherlands: Elsevier. p. 222. ISBN 9780444507631. http://books.google.com/books?id=CE569saGK70C&pg=PA222.
- ^ Chen C-Y, Storr CL, Anthony JC. (2008). "Early-onset drug use and risk for drug dependence problems". Addictive Behaviors 34 (3): 319–22. doi:10.1016/j.addbeh.2008.10.021. PMC 2677076. PMID 19022584. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2677076.
- ^ van Amsterdam J, Opperhuizen A, Koeter M, van den Brink W. (2010). "Ranking the harm of alcohol, tobacco and illicit drugs for the individual and the population". European Addiction Research 16 (4): 202–7. doi:10.1159/000317249. PMID 20606445.
- ^ Nutt DJ, King LA, Saulsbury W, Blakemore C. (2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Lancet 369 (9566): 1047–53. doi:10.1016/S0140-6736(07)60464-4. PMID 17382831.
- ^ Nutt DJ, King LA, Phillips LD. (2010). "Drug harms in the UK: a multicriteria decision analysis". Lancet 376 (9752): 1558–65. doi:10.1016/S0140-6736(10)61462-6. PMID 21036393.
- ^ a b Stamets (1996), pp. 36–41.
- ^ Matsushima Y, Eguchi F, Kikukawa T, Matsuda T. (2009). "Historical overview of psychoactive mushrooms" (PDF). Inflammation and Regeneration 29 (1): 47–58. http://www.jsir.gr.jp/past_journal/2901/0047-0058.pdf.
- ^ Hasler F, Bourquin D, Brenneisen R, Vollenweider FX. (2002). "Renal excretion profiles of psilocin following oral administration of psilocybin: a controlled study in man". Journal of Pharmaceutical and Biomedical Analysis 30 (2): 331–9. doi:10.1016/S0731-7085(02)00278-9. PMID 12191719.
- ^ Baselt RC. (2008). Disposition of Toxic Drugs and Chemicals in Man. Foster City, California: Biomedical Publications. pp. 1346–8. ISBN 0962652377.
- ^ Ballesteros et al. (2006), p. 171.
- ^ Nicholas LG, Ogame K. (2006). Psilocybin Mushroom Handbook: Easy Indoor and Outdoor Cultivation. Oakland, California: Quick American Archives. p. 164. ISBN 9780932551719. http://books.google.com/books?id=HJJmJYCl3HsC&pg=PA164.
- ^ Isbell H, Wolbach AB, Wikler A, Miner EJ. (1961). "Cross tolerance between LSD and psilocybin". Psychopharmacologia 2 (3): 147–59. doi:10.1007/BF00407974. PMID 13717955.
- ^ Abramson HA, Rolo A. (1965). "Lysergic acid diethylamide (LSD-25). 38. Comparison with action of methysergide and psilocybin on test subjects". The Journal of Asthma Research 3 (1): 81–96. doi:10.3109/02770906509106904. PMID 5318626.
- ^ Beck O, Helander A, Karlson-Stiber C, Stephansson N. (1998). "Presence of phenylethylamine in hallucinogenic Psilocybe mushroom: possible role in adverse reactions". Journal of Analytical Toxicology 22 (1): 45–9. PMID 9491968.
- ^ Berge JT. (1999). "Breakdown or breakthrough? A history of European research into drugs and creativity". Journal of Creative Behavior 33 (4): 257–76. ISSN 0022-0175.
- ^ a b c Hasler F, Grimberg U, Benz MA, Huber T, Vollenweider FX. (2004). "Acute psychological and physiological effects of psilocybin in healthy humans: a double-blind, placebo-controlled dose-effect study". Psychopharmacology 172 (2): 145–56. doi:10.1007/s00213-003-1640-6. PMID 14615876.
- ^ Ballesteros et al. (2006), p. 175.
- ^ Studerus E, Kometer M, Hasler F, Vollenweider FX. (20 September, 2010). "Acute, subacute and long-term subjective effects of psilocybin in healthy humans: a pooled analysis of experimental studies". Journal of Psychopharmacology. doi:10.1177/0269881110382466.
- ^ a b MacLean KA, Johnson MW, Griffiths RR. (28 September, 2011). "Mystical experiences occasioned by the hallucinogen psilocybin lead to increases in the personality domain of openness". Journal of Psychopharmacology. doi:10.1177/0269881111420188.
- ^ Quentin A-M. (1960) (in French). La Psilocybine en Psychiatrie Clinique et Experimentale [Psilocybin in Clinical and Experimental Psychiatry] (PhD thesis). Paris, France: Paris University Medical Dissertation.
- ^ See for example:
- Isbell H. (1959). "Comparison of the reactions induced by psilocybin and LSD-25 in man". Psychopharmacologia 1 (1): 29–38. doi:10.1007/BF00408109. PMID 14405870.
- Hollister LE, Prusmack JJ, Paulsen A, Rosenquist N. (1960). "Comparison of three psychotropic drugs (psilocybin, JB-329, and IT-290) in volunteer subjects". Journal of Nervous and Mental Disease 131 (5): 428–34. doi:10.1097/00005053-196011000-00007. PMID 13715375.
- Malitz S, Esecover H, Wilkens B, Hoch PH. (1960). "Some observations on psilocybin, a new hallucinogen, in volunteer subjects". Comprehensive Psychiatry 1: 8–17. doi:10.1016/S0010-440X(60)80045-4. PMID 14420328.
- Rinkel M, Atwell CR, Dimascio A, Brown J. (1960). "Experimental psychiatry. V. Psilocybine, a new psychotogenic drug". New England Journal of Medicine 11 (262): 295–7. doi:10.1056/NEJM196002112620606. PMID 14437505.
- Parashos AJ. (1976). "The psilocybin-induced "state of drunkenness" in normal volunteers and schizophrenics". Behavioral Neuropsychiatry 8 (1–12): 83–6. PMID 1052267.
- ^ Heimann H. (1994). "Experience of time and space in model psychoses". In Pletscher A, Ladewig D (eds.). 50 Years of LSD. Current Status and Perspectives of Hallucinogens. New York, New York: The Parthenon Publishing Group. pp. 59–66. ISBN 1850705690.
- ^ a b Wittmann M, Carter O, Hasler F, Cahn BR, Grimberg U, Spring P, Hell D, Flohr H, Vollenweider FX. (2007). "Effects of psilocybin on time perception and temporal control of behaviour in humans". Journal of Psychopharmacology (Oxford) 21 (1): 50–64. doi:10.1177/0269881106065859. PMID 16714323.
- ^ Wackermann J, Wittmann M, Hasler F, Vollenweider FX. (2008). "Effects of varied doses of psilocybin on time interval reproduction in human subjects". Neuroscience Letters 435 (1): 51–5. doi:10.1016/j.neulet.2008.02.006. PMID 18325673.
- ^ Carter OL, Burr DC, Pettigrew JD, Wallis GM, Hasler F, Vollenweider FX. (2005). "Using psilocybin to investigate the relationship between attention, working memory, and the serotonin 1A and 2A receptors". Journal of Cognitive Neuroscience 17 (10): 1497–508. doi:10.1162/089892905774597191. PMID 16269092.
- ^ Harrington DL, Haaland KY. (1999). "Neural underpinnings of temporal processing: A review of focal lesion, pharmacological, and functional imaging research". Reviews in the Neurosciences 10 (2): 91–116. doi:10.1515/REVNEURO.19220.127.116.11. PMID 10658954.
- ^ Stafford (1992), p. 273.
- ^ Peden NR, Pringle SD, Crooks J. (1982). "The problem of psilocybin mushroom abuse". Human Toxicology 1 (4): 417–24. doi:10.1177/096032718200100408. PMID 7173927.
- ^ Hyde C, Glancy P, Omerod P, Hall D, Taylor GS. (1978). "Abuse of indigenous psilocybin mushrooms: a new fashion and some psychiatric complications". British Journal of Psychiatry 132 (6): 602–4. doi:10.1192/bjp.132.6.602. PMID 566144.
- ^ Mack RB. (1983). "Phenomenally phunny phungi – psilocybin toxicity". New Castle Medical Journal 44 (10): 639–40. PMID 6580536.
- ^ a b Carhart-Harris RL, Nutt DJ. (2010). "User perceptions of the benefits and harms of hallucinogenic drug use: A web-based questionnaire study". Journal of Substance Abuse 15 (4): 283–300. doi:10.3109/14659890903271624.
- ^ Geyer MA. (1998). "Behavioral studies of hallucinogenic drugs in animals: implications for schizophrenia research". Pharmacopsychiatry 31 (Suppl 2): 73–9. doi:10.1055/s-2007-979350. PMID 9754837.
- ^ a b Vollenweider FX, Geyer MA. (2001). "A systems model of altered consciousness: integrating natural and drug-induced psychoses". Brain Research Bulletin 56 (5): 495–507. doi:10.1016/S0361-9230(01)00646-3. PMID 11750795.
- ^ Geyer MA, Vollenweider FX. (2008). "Serotonin research: contributions to understanding psychoses". Trends in Pharmacological Sciences 29 (9): 445–53. doi:10.1016/j.tips.2008.06.006. PMID 19086254.
- ^ Espiard ML, Lecardeur L, Abadie P, Halbecq I, Dollfus S. (2005). "Hallucinogen persisting perception disorder after psilocybin consumption: a case study". European Journal of Psychiatry 20 (5–6): 458–60. doi:10.1016/j.eurpsy.2005.04.008. PMID 15963699.
- ^ Aldurra G, Crayton JW. (2001). "Improvement of hallucinogen persisting perception disorder by treatment with a combination of fluoxetine and olanzapine: case report". Journal of Clinical Psychopharmacology 21 (3): 343–4. doi:10.1097/00004714-200106000-00016. PMID 11386500.
- ^ Myers LS, Watkins SS, Carter TJ. (1998). "Flashbacks in theory and practice" (PDF). The Heffter Review of Psychedelic Research 1: 51–7. http://www.heffter.org/docs/hrireview/01/chapter7.pdf.
- ^ James W. (1997). The Varieties of Religious Experience. New York, New York: Simon & Schuster. ISBN 9780684842974.
- ^ Metzner R. (1998). "Hallucinogenic drugs and plants in psychotherapy and shamanism". Journal of Psychoactive Drugs 40 (4): 333–41. PMID 9924839.
- ^ Pahnke WN, Richards W. (1966). "Implications of LSD and experimental mysticism". Journal of Religion and Health 5 (3): 175–208. doi:10.1007/BF01532646.
- ^ Pahnke WN. (1966). "Drugs and mysticism". International Journal of Parapsychology 8 (2): 295–315.
- ^ a b Griffiths R, Richards W, Johnson M, McCann U, Jesse R. (2008). "Mystical-type experiences occasioned by psilocybin mediate the attribution of personal meaning and spiritual significance 14 months later" (PDF). Journal of Psychopharmacology 22 (6): 621–32. doi:10.1177/0269881108094300. PMC 3050654. PMID 18593735. http://www.csp.org/psilocybin/Hopkins-CSP-Psilocybin2008.pdf.
- ^ Smith H. (2000). Cleansing the Doors of Perception: The Religious Significance of Entheogenic Plants and Chemicals. New York, New York: Jeremy P. Tarcher/Putnam. p. 101. ISBN 9781585420346.
- ^ Doblin (1991), p. 13.
- ^ Doblin (1991), p. 24.
- ^ Richards WA. (2008). "The phenomenology and potential religious import of states of consciousness facilitated by psilocybin". Archive for the Psychology of Religion 30 (1): 189–99. doi:10.1163/157361208X317196.
- ^ Griffiths RR, Richards WA, McCann U, Jesse R. (2006). "Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance" (PDF). Psychopharmacology 187 (3): 268–83. PMID 16826400. http://www.hopkinsmedicine.org/bin/s/m/GriffithsPsilocybin.pdf.
- ^ "Press release: Griffiths psilocybin". Johns Hopkins Medicine. July 11, 2006. http://www.hopkinsmedicine.org/Press_releases/2006/GriffithspsilocybinQ.
- ^ Hood RW Jr. (1975). "The construction and preliminary validation of a measure of reported mystical experience". Journal for the Scientific Study of Religion 14 (1): 29–41. doi:10.2307/1384454. JSTOR 1384454.
- ^ Smith M. (Jul 12, 2006). "Medical News: Psilocybin Viewed as Therapy or Research Tool". Medpagetoday.com. http://www.medpagetoday.com/Psychiatry/GeneralPsychiatry/tb/3721. Retrieved 2011-02-12.
- ^ a b "John Hopkins probes "Sacred" Mushroom Chemical". Newswise.com. June 13, 2011. http://www.newswise.com/articles/view/577702.
- ^ Griffiths RR, Johnson MW, Richards WA, Richards BD, McCann U, Jesse R. (Jun 15, 2011). "Psilocybin occasioned mystical-type experiences: immediate and persisting dose-related effects". Psychopharmacology. doi:10.1007/s00213-011-2358-5. PMID 21674151.
- ^ Wark C, Galliher JF. (2009). "Timothy Leary, Richard Alpert (Ram Dass) and the changing definition of psilocybin". The International Journal on Drug Policy 21 (3): 234–9. doi:10.1016/j.drugpo.2009.08.004. PMID 19744846.
- ^ Brown D. (11 July, 2006). "Drug's mystical properties confirmed". Washington Post. http://www.washingtonpost.com/wp-dyn/content/article/2006/07/10/AR2006071001304.html. Retrieved 2011-09-12.
- ^ Marley (2010), pp. 179–81.
- ^ Moreno FA, Delgado P, Gelenberg AJ. "Effects of Psilocybin in Obsessive-Compulsive Disorder". Multidisciplinary Association for Psychedelic Studies (MAPS). http://www.maps.org/research/psilo/azproto.html. Retrieved 2011-07-23.
- ^ Moreno FA, Wiegand CB, Taitano EK, Delgado PL. (2006). "Safety, tolerability, and efficacy of psilocybin in 9 patients with obsessive-compulsive disorder". Journal of Clinical Psychiatry 67 (11): 1735–40. doi:10.4088/JCP.v67n1110. PMID 17196053.
- ^ a b c Vollenweider FX, Kometer M. (2010). "The neurobiology of psychedelic drugs: implications for the treatment of mood disorders". Nature Reviews Neuroscience 11 (9): 642–51. doi:10.1038/nrn2884. PMID 20717121.
- ^ Prosser S, Wilbourn M. (2003). The Pathology and Pharmacology of Mental Illness (Mental Health Nursing & the Community). Cheltenham, UK: Nelson Thornes Ltd. pp. 55–6. ISBN 9780748753215. http://books.google.com/books?id=GDzKbCg_YbAC&pg=PA55.
- ^ Halker R, Vargas B, Dodick DW. (2010). "Cluster headache: diagnosis and treatment". Seminars in Neurology 30 (2): 175–85. doi:10.1055/s-0030-1249226. PMID 20352587.
- ^ Husid MS. (2007). "Cluster headache: A case-based review of diagnostic and treatment approaches". Current Pain and Headache Reports 10 (2): 117–25. doi:10.1007/s11916-006-0022-2. PMID 16539864.
- ^ Sewell RA, Halpern JH, Pope HG Jr. (2006). "Response of cluster headache to psilocybin and LSD". Neurology 66 (12): 1920–2. doi:10.1212/01.wnl.0000219761.05466.43. PMID 16801660.
- ^ Sun-Edelstein C, Mauskop A. (2011). "Alternative headache treatments: nutraceuticals, behavioral and physical treatments". Headache: the Journal of Head and Face Pain 51 (3): 469–83. doi:10.1111/j.1526-4610.2011.01846.x. PMID 21352222.
- ^ Grob CS, Danforth AL, Chopra GS, Hagerty M, McKay CR, Halberstadt AL, Greer GR. (2011). "Pilot study of psilocybin treatment for anxiety in patients with advanced-stage cancer". Archives of General Psychiatry 68 (1): 71–8. doi:10.1001/archgenpsychiatry.2010.116. PMID 20819978.
- ^ "Psychopharmacology of Psilocybin in Cancer Patients". ClinicalTrials.gov. U.S. National Institutes of Health. 2009. http://www.clinicaltrials.gov/ct2/show/NCT00465595. Retrieved 2011-07-24.
- ^ "Seeking volunteers with a cancer diagnosis to participate in a scientific study of self-exploration and personal meaning". Recruitment notice for psilocybin clinical trial. Johns Hopkins School of Medicine. http://www.bpru.org/cancer/. Retrieved 2009-09-29.
- ^ Johnson MW, Richards WA, Griffiths RR. (2008). "Human hallucinogen research: guidelines for safety" (PDF). Journal of Psychopharmacology 22 (6): 603–20. doi:10.1177/0269881108093587. PMC 3056407. PMID 18593734. http://csp.org/psilocybin/HopkinsHallucinogenSafety2008.pdf.
- ^ a b c d Boire (2002), p. 25.
- ^ Boire (2002), p. 26.
- ^ a b "List of psychotropic substances under international control" (PDF). Vienna, Austria: International Narcotics Control Board. August 2003. http://www.incb.org/pdf/e/list/green.pdf.
- ^ Ballesteros et al. (2006), pp. 178–9.
- ^ Boire (2002), pp. 25–48.
- ^ Frecska E, Luna LE. (2006). "The adverse effects of hallucinogens from intramural perspective". Neuropsychopharmacolia Hungarica 8 (4): 189–200. PMID 17211054.
- Ballesteros S, Ramón MF, Iturralde MJ, Martínez-Arrieta R. (2006). "Natural sources of drugs of abuse: magic mushrooms". In Cole SM. New Research on Street Drugs. New York, New York: Nova Science Publishers. pp. 167–86. ISBN 9781594549618.
- Boire RG. (2002). Sacred Mushrooms and the Law. Berkeley, California: Ronin Publishing. ISBN 9781579510619.
- Doblin R. (1991). "Pahnke's "Good Friday Experiment": A long-term follow-up and methodological critique" (PDF). Journal of Transpersonal Psychology 23 (1): 1–25. http://www.neurosoup.com/pdf/doblin_goodfriday_followup.pdf.
- Marley G. (2010). "Psilocybin: gateway to the soul or just a good high?". Chanterelle Dreams, Amanita Nightmares: The Love, Lore, and Mystique of Mushrooms. White River Junction, Vermont: Chelsea Green Publishing. pp. 163–84. ISBN 1603582142.
- Ott J. (1993). Pharmacotheon: Entheogenic Drugs Their Plant Sources and History. Kennewick, Washington: Natural Products Company. ISBN 9780961423438.
- Stafford PJ. (1992). Psychedelics Encyclopedia (3rd ed.). Berkeley, California: Ronin Publishing. ISBN 0914171518.
- Stamets P. (1996). Psilocybin Mushrooms of the World: An Identification Guide. Berkeley, California: Ten Speed Press. ISBN 0898158397.
- Wurst M, Kysilka R, Flieger M. (2002). "Psychoactive tryptamines from Basidiomycetes". Folia Microbiologica 47 (1): 3–27. doi:10.1007/BF02818560. PMID 11980266.
- Hopkins/CSP research findings and media reports, 2006, 2008, 2011
- "Risk assessment report relating to paddos (psilocin and psilocybin)"—2000 report by the Dutch government
- MAPS Psilocybin research
- Clusterbusters Psilocybin as cluster headache treatment
- JHU Official Study Website
2006 Johns Hopkins experiment
- "Hopkins Scientists Show Hallucinogen in Mushrooms Creates Universal 'Mystical' Experience", Johns Hopkins Medicine news release, July 11, 2006.
- "Tripping Out: Scientists Study Mystical Effects of Mushrooms" by Joy Victory, Bharathi Radhakrishnan, and Andrea Carter, ABC News (online), July 11, 2006. ABC News video report of the study.
2008 Follow-up to Johns Hopkins experiment
- "Spiritual Effects of Hallucinogens Persist, Johns Hopkins Researchers Report", Johns Hopkins Medicine news release, July 1, 2008.
- "Sacred Intentions: Inside the Johns Hopkins Psilocybin Studies" by Michael M. Hughes, City Paper, October 8, 2008.
Serotonergics 5-HT1 receptor ligandsAgonists: Azapirones: Alnespirone • Binospirone • Buspirone • Enilospirone • Eptapirone • Gepirone • Ipsapirone • Perospirone • Revospirone • Tandospirone • Tiospirone • Umespirone • Zalospirone; Antidepressants: Etoperidone • Nefazodone • Trazodone • Vortioxetine; Antipsychotics: Aripiprazole • Asenapine • Clozapine • Quetiapine • Ziprasidone; Ergolines: Dihydroergotamine • Ergotamine • Lisuride • Methysergide • LSD; Tryptamines: 5-CT • 5-MeO-DMT • 5-MT • Bufotenin • DMT • Indorenate • Psilocin • Psilocybin; Others: 8-OH-DPAT • Adatanserin • Befiradol • BMY-14802 • Cannabidiol • Dimemebfe • Ebalzotan • Eltoprazine • F-11,461 • F-12,826 • F-13,714 • F-14,679 • F-15,063 • F-15,599 • Flesinoxan • Flibanserin • Lesopitron • LY-293,284 • LY-301,317 • MKC-242 • NBUMP • Osemozotan • Oxaflozane • Pardoprunox • Piclozotan • Rauwolscine • Repinotan • Roxindole • RU-24,969 • S 14,506 • S-14,671 • S-15,535 • Sarizotan • SSR-181,507 • Sunepitron • U-92,016-A • Urapidil • Vilazodone • Xaliproden • Yohimbine
Antagonists: Antipsychotics: Iloperidone • Risperidone • Sertindole; Beta blockers: Alprenolol • Cyanopindolol • Iodocyanopindolol • Oxprenolol • Pindobind • Pindolol • Propranolol • Tertatolol; Others: AV965 • BMY-7,378 • CSP-2503 • Dotarizine • Flopropione • GR-46611 • Isamoltane • Lecozotan • Mefway • Metitepine/Methiothepin • MPPF • NAN-190 • PRX-00023 • Robalzotan • S-15535 • SB-649,915 • SDZ 216-525 • Spiperone • Spiramide • Spiroxatrine • UH-301 • WAY-100,135 • WAY-100,635 • XylamidineAgonists: Lysergamides: Dihydroergotamine • Ergotamine • Methysergide; Piperazines: Eltoprazine • TFMPP; Triptans: Avitriptan • Eletriptan • Sumatriptan • Zolmitriptan; Tryptamines: 5-CT • 5-MT; Others: CGS-12066A • CP-93,129 • CP-94,253 • CP-135,807 • RU-24,969
Antagonists: Lysergamides: Metergoline; Others: AR-A000002 • Elzasonan • GR-127,935 • Isamoltane • Metitepine/Methiothepin • SB-216,641 • SB-224,289 • SB-236,057 • YohimbineAgonists: Lysergamides: Dihydroergotamine • Methysergide; Triptans: Almotriptan • Avitriptan • Eletriptan • Frovatriptan • Naratriptan • Rizatriptan • Sumatriptan • Zolmitriptan; Tryptamines: 5-CT • 5-Ethyl-DMT • 5-MT • 5-(Nonyloxy)tryptamine; Others: CP-135,807 • CP-286,601 • GR-46611 • L-694,247 • L-772,405 • PNU-109,291 • PNU-142,633
Antagonists: Lysergamides: Metergoline; Others: Alniditan • BRL-15,572 • Elzasonan • GR-127,935 • Ketanserin • LY-310,762 • LY-367,642 • LY-456,219 • LY-456,220 • Metitepine/Methiothepin • Ritanserin • Yohimbine • Ziprasidone
5-HT2 receptor ligandsAgonists: Lysergamides: ALD-52 • Ergometrine • Lisuride • LA-SS-Az • LSD • LSD-Pip • Lysergic acid 2-butyl amide • Lysergic acid 3-pentyl amide • Methysergide; Phenethylamines: 25I-NBF • 25I-NBMD • 25I-NBOH • 25I-NBOMe • 2C-B • 2C-B-FLY • 2CB-Ind • 2C-C-NBOMe • 2C-E • 2C-I • 2C-TFM-NBOMe • 2C-T-2 • 2C-T-7 • 2C-T-21 • 2CBCB-NBOMe • 2CBFly-NBOMe • Bromo-DragonFLY • DOB • DOC • DOI • DOM • MDA • MDMA • Mescaline • TCB-2 • TFMFly; Piperazines: BZP • Quipazine • TFMPP; Tryptamines: 5-CT • 5-MeO-α-ET • 5-MeO-α-MT • 5-MeO-DET • 5-MeO-DiPT • 5-MeO-DMT • 5-MeO-DPT • 5-MT • α-ET • α-Methyl-5-HT • α-MT • Bufotenin • DET • DiPT • DMT • DPT • Psilocin • Psilocybin; Others: AL-34662 • AL-37350A • Dimemebfe • Medifoxamine • Oxaflozane • PNU-22394 • RH-34
Antagonists: Atypical antipsychotics: Amperozide • Aripiprazole • Carpipramine • Clocapramine • Clozapine • Gevotroline • Iloperidone • Melperone • Mosapramine • Olanzapine • Paliperidone • Pimozide • Quetiapine • Risperidone • Sertindole • Ziprasidone • Zotepine; Typical antipsychotics: Loxapine • Pipamperone; Antidepressants: Amitriptyline • Amoxapine • Aptazapine • Etoperidone • Mianserin • Mirtazapine • Nefazodone • Teniloxazine • Trazodone; Others: 5-I-R91150 • AC-90179 • Adatanserin • Altanserin • AMDA • APD-215 • Blonanserin • Cinanserin • CSP-2503 • Cyproheptadine • Deramciclane • Dotarizine • Eplivanserin • Esmirtazapine • Fananserin • Flibanserin • Ketanserin • KML-010 • Lubazodone • Mepiprazole • Metitepine/Methiothepin • Nantenine • Pimavanserin • Pizotifen • Pruvanserin • Rauwolscine • Ritanserin • S-14,671 • Sarpogrelate • Setoperone • Spiperone • Spiramide • SR-46349B • Volinanserin • Xylamidine • YohimbineAgonists: Oxazolines: 4-Methylaminorex • Aminorex; Phenethylamines: Chlorphentermine • Cloforex • DOB • DOC • DOI • DOM • Fenfluramine • MDA • MDMA • Norfenfluramine; Tryptamines: 5-CT • 5-MT • α-Methyl-5-HT; Others: BW-723C86 • Cabergoline • mCPP • Pergolide • PNU-22394 • Ro60-0175
Antagonists: Agomelatine • Asenapine • EGIS-7625 • Ketanserin • Lisuride • LY-272,015 • Metitepine/Methiothepin • PRX-08066 • Rauwolscine • Ritanserin • RS-127,445 • Sarpogrelate • SB-200,646 • SB-204,741 • SB-206,553 • SB-215,505 • SB-221,284 • SB-228,357 • SDZ SER-082 • Tegaserod • YohimbineAgonists: Phenethylamines: 2C-B • 2C-E • 2C-I • 2C-T-2 • 2C-T-7 • 2C-T-21 • DOB • DOC • DOI • DOM • MDA • MDMA • Mescaline; Piperazines: Aripiprazole • mCPP • TFMPP; Tryptamines: 5-CT • 5-MeO-α-ET • 5-MeO-α-MT • 5-MeO-DET • 5-MeO-DiPT • 5-MeO-DMT • 5-MeO-DPT • 5-MT • α-ET • α-Methyl-5-HT • α-MT • Bufotenin • DET • DiPT • DMT • DPT • Psilocin • Psilocybin; Others: A-372,159 • AL-38022A • CP-809,101 • Dimemebfe • Lorcaserin• Medifoxamine • MK-212 • Org 12,962 • ORG-37,684 • Oxaflozane • PNU-22394 • Ro60-0175 • Ro60-0213 • Vabicaserin • WAY-629 • WAY-161,503 • YM-348
Antagonists: Atypical antipsychotics: Clozapine • Iloperidone • Melperone • Olanzapine • Paliperidone • Pimozide • Quetiapine • Risperidone • Sertindole • Ziprasidone • Zotepine; Typical antipsychotics: Chlorpromazine • Loxapine • Pipamperone; Antidepressants: Agomelatine • Amitriptyline • Amoxapine • Aptazapine • Etoperidone • Fluoxetine • Mianserin • Mirtazapine • Nefazodone • Nortriptyline • Tedatioxetine • Trazodone; Others: Adatanserin • Cinanserin • Cyproheptadine • Deramciclane • Dotarizine • Eltoprazine • Esmirtazapine • FR-260,010 • Ketanserin • Ketotifen • Latrepirdine • Metitepine/Methiothepin • Methysergide • Pizotifen • Ritanserin • RS-102,221 • S-14,671 • SB-200,646 • SB-206,553 • SB-221,284 • SB-228,357 • SB-242,084 • SB-243,213 • SDZ SER-082 • Xylamidine
5-HT3, 5-HT4, 5-HT5, 5-HT6, 5-HT7 ligandsAgonists: Piperazines: BZP • Quipazine; Tryptamines: 2-Methyl-5-HT • 5-CT; Others: Chlorophenylbiguanide • Butanol • Ethanol • Halothane • Isoflurane • RS-56812 • SR-57,227 • SR-57,227-A • Toluene • Trichloroethane • Trichloroethanol • Trichloroethylene • YM-31636
Antagonists: Antiemetics: AS-8112 • Alosetron • Azasetron • Batanopride • Bemesetron • Cilansetron • Dazopride • Dolasetron • Granisetron • Lerisetron • Ondansetron • Palonosetron • Ramosetron • Renzapride • Tropisetron • Zacopride • Zatosetron; Atypical antipsychotics: Clozapine • Olanzapine • Quetiapine; Tetracyclic antidepressants: Amoxapine • Mianserin • Mirtazapine; Others: CSP-2503 • ICS-205,930 • MDL-72,222 • Memantine • Nitrous Oxide • Ricasetron • Sevoflurane • Tedatioxetine • Thujone • Vortioxetine • XenonAgonists: Gastroprokinetic Agents: Cinitapride • Cisapride • Dazopride • Metoclopramide • Mosapride • Prucalopride • Renzapride • Tegaserod • Velusetrag • Zacopride; Others: 5-MT • BIMU8 • CJ-033,466 • PRX-03140 • RS-67333 • RS-67506 • SL65.0155 • Antagonists: GR-113,808 • GR-125,487 • L-Lysine • Piboserod • RS-39604 • RS-67532 • SB-203,186 • SB-204,070Agonists: Lysergamides: Dihydroergotamine • Ergotamine • Lisuride • LSD • Mesulergine • Metergoline • Methysergide; Tryptamines: 2-Methyl-5-HT • 5-BT • 5-CT • 5-MT • Bufotenin • E-6801 • E-6837 • EMD-386,088 • EMDT • LY-586,713 • Tryptamine; Others: WAY-181,187 • WAY-208,466
Antagonists: Antidepressants: Amitriptyline • Amoxapine • Clomipramine • Doxepin • Mianserin • Nortriptyline; Atypical antipsychotics: Aripiprazole • Asenapine • Clozapine • Fluperlapine • Iloperidone • Olanzapine • Tiospirone; Typical antipsychotics: Chlorpromazine • Loxapine; Others: BGC20-760 • BVT-5182 • BVT-74316 • Cerlapirdine • EGIS-12,233 • GW-742,457 • Ketanserin • Latrepirdine • Lu AE58054 • Metitepine/Methiothepin • MS-245 • PRX-07034 • Ritanserin • Ro04-6790 • Ro 63-0563 • SB-258,585 • SB-271,046 • SB-357,134 • SB-399,885 • SB-742,457Agonists: Lysergamides: LSD; Tryptamines: 5-CT • 5-MT • Bufotenin; Others: 8-OH-DPAT • AS-19 • Bifeprunox • E-55888 • LP-12 • LP-44 • RU-24,969 • Sarizotan
Antagonists: Lysergamides: 2-Bromo-LSD • Bromocriptine • Dihydroergotamine • Ergotamine • Mesulergine • Metergoline • Methysergide; Antidepressants: Amitriptyline • Amoxapine • Clomipramine • Imipramine • Maprotiline • Mianserin; Atypical antipsychotics: Amisulpride • Aripiprazole • Clozapine • Olanzapine • Risperidone • Sertindole • Tiospirone • Ziprasidone • Zotepine; Typical antipsychotics: Chlorpromazine • Loxapine; Others: Butaclamol • EGIS-12,233 • Ketanserin • LY-215,840 • Metitepine/Methiothepin • Pimozide • Ritanserin • SB-258,719 • SB-258,741 • SB-269,970 • SB-656,104 • SB-656,104-A • SB-691,673 • SLV-313 • SLV-314 • Spiperone • SSR-181,507
Reuptake inhibitorsSelective serotonin reuptake inhibitors (SSRIs): Alaproclate • Citalopram • Dapoxetine • Desmethylcitalopram • Desmethylsertraline • Escitalopram • Femoxetine • Fluoxetine • Fluvoxamine • Indalpine • Ifoxetine • Litoxetine • Lubazodone • Panuramine • Paroxetine • Pirandamine • RTI-353 • Seproxetine • Sertraline • Tedatioxetine • Vilazodone • Vortioxetine • Zimelidine; Serotonin-norepinephrine reuptake inhibitors (SNRIs): Bicifadine • Desvenlafaxine • Duloxetine • Eclanamine • Levomilnacipran • Milnacipran • Sibutramine • Venlafaxine; Serotonin-norepinephrine-dopamine reuptake inhibitors (SNDRIs): Brasofensine • Diclofensine • DOV-102,677 • DOV-21,947 • DOV-216,303 • NS-2359 • SEP-225289 • SEP-227,162 • Tesofensine; Tricyclic antidepressants (TCAs): Amitriptyline • Butriptyline • Cianopramine • Clomipramine • Desipramine • Dosulepin • Doxepin • Imipramine • Lofepramine • Nortriptyline • Pipofezine • Protriptyline • Trimipramine; Tetracyclic antidepressants (TeCAs): Amoxapine; Piperazines: Nefazodone • Trazodone; Antihistamines: Brompheniramine • Chlorphenamine • Diphenhydramine • Mepyramine/Pyrilamine • Pheniramine • Tripelennamine; Opioids: Pethidine • Methadone • Propoxyphene; Others: Cocaine • CP-39,332 • Cyclobenzaprine • Dextromethorphan • Dextrorphan • EXP-561 • Fezolamine • Mesembrine • Nefopam • PIM-35 • Pridefine • Roxindole • SB-649,915 • Ziprasidone Releasing agentsAminoindanes: 5-IAI • AMMI • ETAI • MDAI • MDMAI • MMAI • TAI; Aminotetralins: 6-CAT • 8-OH-DPAT • MDAT • MDMAT; Oxazolines: 4-Methylaminorex • Aminorex • Clominorex • Fluminorex; Phenethylamines (also Amphetamines, Cathinones, Phentermines, etc): 2-Methyl-MDA • 4-CAB • 4-FA • 4-FMA • 4-HA • 4-MTA • 5-APDB • 5-Methyl-MDA • 6-APDB • 6-Methyl-MDA • AEMMA • Amiflamine • BDB • BOH • Brephedrone • Butylone • Chlorphentermine • Cloforex • Amfepramone • Metamfepramone • DFMDA • DMA • DMMA • EBDB • EDMA • Ethylone • Etolorex • Fenfluramine (Dexfenfluramine) • Flephedrone • IAP • IMP • Lophophine • MBDB • MDA • MDEA • MDHMA • MDMA • MDMPEA • MDOH • MDPEA • Mephedrone • Methedrone • Methylone • MMA • MMDA • MMDMA • MMMA • NAP • Norfenfluramine • 4-TFMA • pBA • pCA • pIA • PMA • PMEA • PMMA • TAP; Piperazines: 2C-B-BZP • 2-BZP • 3-MeOPP • BZP • DCPP • MBZP • mCPP • MDBZP • MeOPP • Mepiprazole • pCPP • pFPP • pTFMPP • TFMPP; Tryptamines: 4-Methyl-αET • 4-Methyl-αMT • 5-CT • 5-MeO-αET • 5-MeO-αMT • 5-MT • αET • αMT • DMT • Tryptamine (itself); Others: Indeloxazine • Tramadol • Viqualine Enzyme inhibitorsAGN-2979 • FenclonineNonselective: Benmoxin • Caroxazone • Echinopsidine • Furazolidone • Hydralazine • Indantadol • Iproclozide • Iproniazid • Isocarboxazid • Isoniazid • Linezolid • Mebanazine • Metfendrazine • Nialamide • Octamoxin • Paraxazone • Phenelzine • Pheniprazine • Phenoxypropazine • Pivalylbenzhydrazine • Procarbazine • Safrazine • Tranylcypromine; MAO-A Selective: Amiflamine • Bazinaprine • Befloxatone • Befol • Brofaromine • Cimoxatone • Clorgiline • Esuprone • Harmala alkaloids (Harmine, Harmaline, Tetrahydroharmine, Harman, Norharman, etc) • Methylene Blue • Metralindole • Minaprine • Moclobemide • Pirlindole • Sercloremine • Tetrindole • Toloxatone • Tyrima OthersOthers Tryptamines
1-(2-Dimethylaminoethyl)dihydropyrano(3,2-e)indole • 2-Methyl-5-HT • 4-Acetoxy-DET • 4-Acetoxy-DIPT • 4-Acetoxy-DMT • 4-HO-αMT • 4-HO-DIPT • 4-HO-MET • 4-MeO-DMT • 4-Methyl-αET • 4-Methyl-αMT • 5-Benzyloxytryptamine • 5-Bromo-DMT • 5-Carboxamidotryptamine • 5-Ethoxy-αMT • 5-Fluoro-αMT • 5-HO-αMT • 5-HTP • 5-Ethoxy-DMT • 5-Ethyl-DMT • 5-Fluoro-DMT • 5-Methyl-DMT • 5-Methoxytryptamine • 5-MeO-7,N,N-TMT • 5-Methyl-αET • 5-MeO-αET • 5-MeO-αMT • 5-MeO-DALT • 5-MeO-DET • 5-MeO-DIPT • 5-MeO-DMT • 5-MeO-DPT • 5-MeO-MALT • 5-MeO-MIPT • 5,7-Dihydroxytryptamine • 5-(Nonyloxy)tryptamine • 6-Fluoro-αMT • 7-Methyl-αET • 7-Methyl-DMT • αET • αMT • Aeruginascin • AL-37350A • BW-723C86 • Baeocystin • Bufotenidine • Bufotenin • DALT • Desformylflustrabromine • DET • DiPT • DMT • DPT • Ethocybin • EiPT • EMDT • EPT • Ethocin • FGIN-127 • FGIN-143 • Ibogaine • Indorenate • Iprocin • MET • MiPT • Miprocin • Melatonin • MS-245 • NAS • NMT • Norbaeocystin • Normelatonin • Oxypertine • PiPT • Psilocin • Psilocybin • Rizatriptan • Serotonin • Sumatriptan • Tryptamine • Tryptophan • Yohimbine • Yuremamine • Zolmitriptan
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Psilocybin — [griechisch] das, s, Indolalkaloid, das in Form wasserlöslicher farbloser Kristalle aus dem mexikanischen Rauschpilz Psilocybe mexicana gewonnen wird (Psilocybingehalt etwa 0,3 %). Psilocybin ist neben Haschisch, Mescalin und LSD das… … Universal-Lexikon
psilocybin — 1958, from Mod.L. psilocybe, name of a Central Amer. species of mushroom, from Gk. psilos bare (akin to psen to rub ) + kybe head … Etymology dictionary
psilocybin — [sī΄lə sī′bin, sil΄əsī′bin] n. [< ModL Psilocybe < Gr psilos, bare (akin to psēn, to rub: see PSORIASIS) + kybē, head + IN1] a hallucinogenic drug obtained from a fungus (genus Psilocybe, esp. P. mexicana) … English World dictionary
Psilocybin — Strukturformel Allgemeines Name Psilocybin Andere … Deutsch Wikipedia
Psilocybin — A hallucinogenic or entheogenic alkaloid (4 phosphoryloxyN, N dimethyltryptamine) of the tryptamine family present in many species of fungi, the best known being the genus Psilocybe, including Psilocybe cubensis and Psilocybe semilanceata… … Historical dictionary of shamanism
psilocybin — noun Etymology: New Latin Psilocybe, fungus genus + 1 in Date: 1958 a hallucinogenic indole C12H17N2O4P obtained from a fungus (as Psilocybe mexicana or P. cubensis syn. Stropharia cubensis) … New Collegiate Dictionary
psilocybin — /sil euh suy bin, suy leuh /, n. Pharm. a hallucinogenic crystalline solid, C12H17N2O4P, obtained from the mushroom Psilocybe mexicana. [1955 60; < NL Psilocyb(e) genus of mushrooms ( < Gk psiló(s) bare + kýbe head) + IN2] * * * … Universalium
psilocybin — noun /saɪləˈsaɪbɪn/ A hallucinogenic alkaloid, C₁₂H₁₅N₂O·H₂PO₃, present in several species of Central American mushroom and producing effects similar to LSD. See Also: psilocin, Psilocybe semilanceata … Wiktionary
psilocybin — The N′,N′ dimethyl derivative of 4 hydroxytryptamine; obtained from the fruiting bodies of the fungus Psilocybe mexicana and other species of Psilocybe and Stropharia. P. is a congener of 5 hydroxytryptamine, with striking central nervous system… … Medical dictionary
psilocybin — saÉªlÉ™ saÉªbÉªn n. hallucinogenic drug derived from a particular species of mushroom … English contemporary dictionary