Muscimol

Natural occurrence

The main natural sources of muscimol are fungi of the genus Amanita, such as Amanita muscaria (fly agaric) and Amanita pantherina (panther cap). It is produced in the mushrooms along with muscarine (which is present in trace amounts and it is not active), muscazone, and ibotenic acid. In Amanita muscaria, the layer just below the skin of the cap contains the highest amount of muscimol, and is therefore the most psychoactive portion.

Use and effects

The properties and effects of muscimol in humans have been limitedly assessed in clinical studies. It has been assessed in these studies at doses of 5 to 15mg orally. The oral threshold dose of muscimol is approximately 6mg, while the psychoactive dose range has been said to range from approximately 8 to 15mg. As little as 1g of dried Amanita muscaria button may contain this amount of muscimol, although the potency varies greatly among mushrooms. According to Jonathan Ott, a 15mg dose is "psychoptic" while a 20mg dose is "visionary". The onset of action of muscimol, via isolated muscimol or Amanita muscaria consumption orally, is between 30minutes and 2hours, with peak effects occurring after 1 to 3hours. The duration is 4 to 8hours, but some effects may persist for up to 24hours. In one publication, the effects of muscimol were described as follows:

: "Waser (1967) describes the effects of self-administration of 10–15 mg. of muscimol as '. . . intense hallucinations as with LSD were missing . . . there resulted considerable disturbances of psychic functions, such as orientation in space and time, visual perception, process of thinking, speech, and some new psychic phenomena of illusions and echo pictures'. Higher doses tended to produce severe intoxication in man, with painful muscular twitching, considerable agitation, and vivid hallucinations."

The effects of muscimol in humans in different studies have been found to include sedation, dizziness, incoordination, relaxation, reduced anxiety, mood improvement, sleep, rich dreaming, difficulty speaking, impaired attention, focus, and concentration, impaired learning, confusion, loss of appetite, stimulation, agitation, hallucinogenic effects, echo-like pseudohallucinations (visual and auditory, vivid hallucinations, psychosis, and delirium. At higher doses, coma, seizures, and death can occur. Physical effects of muscimol can include muscle twitching, flushing, slightly increased blood pressure, nausea, vomiting, abdominal pain, and diarrhea, among others. After-effects have been reported to include fatigue, inactivity, and headache and migraine. Muscimol can increase prolactin and growth hormone levels.

Muscimol is said to have similar effects on sleep in rodents as the related experimental pharmaceutical drug gaboxadol (THIP). In humans, gaboxadol decreases sleep onset latency, increases sleep duration, increases slow wave sleep (SWS) and slow wave activity (SWA), and does not suppress REM sleep. The effects of muscimol and gaboxadol on sleep differ from those of widely used GABAA receptor positive allosteric modulators like benzodiazepines and Z-drugs, which can instead disrupt SWS and SWA despite improving sleep onset and duration. Although muscimol and gaboxadol have similar effects on sleep, muscimol has additionally been found to increase REM sleep unlike gaboxadol.

Ibotenic acid, a prodrug of muscimol, is active at doses of approximately 20 to 100mg orally in humans. About 10 to 20% of ibotenic acid is said to be converted into muscimol following decarboxylation.

Toxicity and overdose

The toxicity and safety profile of muscimol has been studied in various contexts, both experimental and clinical. The median lethal dose (LD50) in mice is 3.8mg/kg s.c, 2.5mg/kg i.p. The LD50 in rats is 4.5mg/kg i.v, 45 mg/kg orally. A study on non-human primates indicated that muscimol, when administered in escalating doses, caused reversible hyperkinesia and dyskinesias at higher doses (up to 88.8 mM), but no long-term toxicity was observed on histological examination. Muscimol has shown potential as an anticonvulsant, blocking seizures induced by various agents in animal models without causing significant toxicity at therapeutic doses. Muscimol exhibits dose-dependent effects with higher doses leading to significant, but reversible, central nervous system symptoms. The dose of muscimol that is thought to be potentially fatal in humans is 90mg, which is 15times its threshold active dose of 6mg.

Interactions

The actions and effects of muscimol may be potentiated by benzodiazepines such as diazepam.

Pharmacology

Pharmacodynamics

Muscimol is a potent GABAA receptor full agonist, activating the receptor for the brain's principal inhibitory neurotransmitter, γ-aminobutyric acid (GABA). Muscimol binds to the same site on the GABAA receptor complex as GABA itself, unlike other GABAergic drugs such as barbiturates, benzodiazepines, and Z-drugs, which interact with separate allosteric sites. GABAA receptors are widely distributed in the brain, so when muscimol is administered, it alters neuronal activity in multiple regions including the cerebral cortex, hippocampus, and cerebellum. By mimicking GABA, muscimol activates these receptors, leading to the opening of chloride channels and subsequent hyperpolarization of neurons. This results in decreased neuronal excitability, which is crucial for maintaining the balance between excitation and inhibition in the central nervous system.

Muscimol shows relatively uniform effects on GABAA receptors of differing subunit compositions. However, it was found to act as a superagonist of extrasynaptic α4β3δ subunit-containing GABAA receptors ( = 120 to 140% relative to GABA). This was found to be due to reduced receptor desensitization with muscimol compared to GABA. Subsequent research has found that muscimol is a preferential agonist of the relatively small population of δ subunit-containing GABAA receptors and that these receptors have a substantial contribution to its effects. In contrast to muscimol, benzodiazepines and Z-drugs do not activate δ subunit-containing GABAA receptors. On the other hand, alcohol is known to selectively potentiate δ subunit-containing extrasynaptic GABAA receptors analogously to muscimol.

While muscimol is often thought of as a selective GABAA agonist with exceptionally high affinity to δ subunit-containing GABAA receptors, it is also a potent partial agonist of the GABAA-ρ receptor, and so its range of effects results from a combined action on more than one GABAA receptor subtype. In fact, it is more potent as a partial agonist of the GABAA-ρ receptor than as a GABAA receptor agonist. Muscimol has been said to be inactive at the GABAB receptor. However, a subsequent study reported that muscimol may have GABAB receptor-mediated inhibitory activity, although more research is needed to further characterize this activity. Muscimol is inactive in terms of affecting GABA transaminase (GABA-T). There is little evidence that muscimol interacts with other biological targets besides the GABA receptors and the GABA transporters.

In animals, muscimol produces central depression, sedation, analgesia, anxiolysis, anticonvulsant effects, neuroprotective effects, and anesthesia, among other effects. In rodent drug discrimination studies, muscimol and gaboxadol fully generalize between each other, but generalization between benzodiazepines like diazepam does not occur. These findings suggest that muscimol and gaboxadol have differing interoceptive effects from those of benzodiazepines. During a test involving rabbits connected to an EEG, muscimol presented with a distinctly synchronized EEG tracing. This is substantially different from serotonergic psychedelics like psilocybin, with which brainwave patterns generally show a desynchronization. In higher doses (2mg/kg via IV), the EEG will show characteristic spikes.

Pharmacokinetics

The pharmacokinetics of muscimol in humans have been very limitedly studied. Pharmacokinetic parameters such as bioavailability, volume of distribution, plasma protein binding, and elimination half-life are unavailable.

Absorption

Muscimol is readily absorbed in the gastrointestinal tract when taken orally.

Distribution

The brain tissue distribution of muscimol in rats has been studied. Muscimol rapidly enters and unevenly distributes in rat brain, especially in the substantia nigra, colliculi, and hypothalamus. Muscimol crosses the blood–brain barrier and hence is centrally active. This has been said to likely be mediated by active transport via the high-affinity GABA uptake system and other amino acid transporters. Although muscimol crosses the blood–brain barrier, it does so relatively poorly and far less readily than gaboxadol.

Metabolism

Muscimol is known to be metabolized via transamination by GABA transaminase (GABA-T). Ibotenic acid is a prodrug of muscimol via decarboxylation. However, it has been said that muscimol can also be converted back into ibotenic acid via glutamate decarboxylase. The metabolites of muscimol have not been identified, but might contribute to the toxicity of muscimol.

Elimination

Muscimol is excreted by the kidneys into urine. It is excreted partially unmetabolized. This has been taken advantage of by Siberian practitioners of the traditional entheogenic use of Amanita muscaria via recycling of muscimol in urine.

The elimination half-life of muscimol in humans is unknown. The closely related drug gaboxadol (THIP), which is a cyclized derivative of muscimol, has an elimination half-life in humans of 1.5 to 2hours. In rodents, the half-life of gaboxadol was about twice as long as that of muscimol. The drug is said to be more resistant to metabolism than muscimol, for instance not being a substrate for GABA-T.

Chemistry

Structure

Muscimol was first isolated from Amanita pantherina by Onda in 1964, and thought to be an amino acid or peptide. Structure was then elucidated by Takemoto, Eugster, and Bowden. Muscimol is a semi-rigid isoxazole containing both alcohol and aminomethyl substituents. Muscimol is commonly portrayed as a tautomer, where it adopts an amide-like configuration. It is also commonly shown as a zwitterion.

Properties

Muscimol is a zwitterion at physiological pH. Its predicted log P of –1.4 to –2.2. The drug's log P is similar to that of γ-aminobutyric acid (GABA).

Isolation

Muscimol can be extracted from the flesh of the Amanita muscaria by treatment with boiling water, followed by rapid cooling, and further treatment with a basic resin. This is washed with water, and eluted with acetic acid using column chromatography. The eluate is freeze dried, dissolved in water, and passed down a column of cellulose phosphate. A subsequent elution with ammonium hydroxide and recrystallization from alcohol results in pure muscimol.

In instances where pure muscimol is not required, such as recreational or spiritual use, a crude extract is often prepared by simmering dried Amanita muscaria in water for 30minutes.

Synthesis

Several chemical syntheses of muscimol have been published.

Analogues

Analogues of muscimol include γ-aminobutyric acid (GABA), ibotenic acid, dihydromuscimol, thiomuscimol, piperidine-4-sulphonic acid (P4S), gaboxadol (THIP), 4-AHP, 4-PIOL, isonipecotic acid, guvacine, isoguvacine, THPO, nipecotic acid, and tiagabine, among others. The structural requirements for GABAA receptor binding and activation are very strict, so relatively few high-efficacy GABAA receptor agonists are known.

History

Amanita muscaria has been used by humans as a psychoactive drug since ancient times. Muscimol was isolated from Amanita muscaria independently by three different research groups in 1964 and 1965. It was synthesized by Gagneux and colleagues in 1965. The chemical structure of muscimol, along with that of ibotenic acid, was published by Conrad Eugster at the University of Zurich in 1967.

Its structural similarity to the neurotransmitter γ-aminobutyric acid (GABA) was quickly recognized and muscimol was shown to have GABA-like actions by Graham Johnston and colleagues in 1968. Subsequently, its actions were shown to be reversed by the GABA receptor antagonist bicuculline in 1971.

The effects of muscimol in humans were studied and described by Waser in 1967. Later, ethnobotanist Jonathan Ott further described the effects of muscimol, via Amanita pantherina consumption, in 1976.

Danish medicinal chemist Povl Krogsgaard-Larsen and colleagues studied muscimol and synthetic analogues over several decades starting in the 1970s. Other GABAA receptor ligands, such as gaboxadol (THIP) and 4-PIOL, and GABA transporter modulators, such as nipecotic acid and tiagabine, have been derived from muscimol. Many muscimol analogues were developed by Krogsgaard-Larsen and colleagues.

Muscimol was encountered online as a novel designer drug in 2023.

Society and culture

Legal status

Muscimol is not a controlled substance and is unregulated in most of the world.

Australia

Muscimol is considered a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015). A Schedule 9 substance is a substance "which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities."

Poland

Muscimol and ibotenic acid are both considered as novel psychoactive substances in Poland as of 2024. Possessing or selling them is illegal.

United States

Neither Amanita muscaria nor muscimol is considered a controlled substance by the Federal government of the United States. The United States Food and Drug Administration (FDA) has deemed Amanita muscaria and its constituents, including muscimol, unapproved for conventional foods and is also evaluating their use in dietary supplements. Agriculture regulators in Florida actioned against one seller of Amanita products after the agency had determined such products were considered adulterated under state law.

Muscimol may be regulated on a state level. Louisiana State Act 159 banned the possession and cultivation of the Amanita muscaria except for ornamental or aesthetic purposes. Except as a constituent of lawfully manufactured food or dietary supplements, the act outlaws preparations of the Amanita muscaria intended for human consumption, including muscimol.

Research

Muscimol has been clinically studied for a number of potential medical uses. It was assessed in small clinical studies in the treatment of Huntington's disease, tardive dyskinesia, and schizophrenia in the 1970s but was not found to be useful for these indications. Another study evaluated muscimol in schizophrenics with tardive dyskinesia in 1992. Studies also assessed the biochemical effects of muscimol in humans in the late 1970s and early 1980s.

According to Povl Krogsgaard-Larsen, muscimol was too toxic and non-selective and as such was not developed for use as a pharmaceutical drug. Instead, the synthetic analogue gaboxadol (THIP), which was more selective and less toxic, was developed.

In 2019, a phase 1 clinical trial of muscimol for drug-resistant epilepsy was published. It has also been formally investigated for potential treatment of Alzheimer's disease and Parkinson's disease. A 2023 systematic review and meta-analysis of 22preclinical studies found that muscimol reduces neuropathic pain in animals, with effects beginning within 15minutes and lasting up to 3hours.

Muscimol has never been approved as a pharmaceutical drug for any use anywhere in the world.

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