Discussion: Ingestion of ibotenic acid/muscimol containing mushrooms often produces a syndrome with GI upset, CNS excitation, and CNS depression either alone or in combination. Ingestion of AP was associated with a higher rate of symptoms compared to AM.

Ibotenic acid is a non-proteinogenic alpha-amino acid. It has a role as a neurotoxin. A neurotoxic isoxazole (similar to KAINIC ACID and MUSCIMOL) found in AMANITA mushrooms. It causes motor depression, ataxia, and changes in mood, perceptions and feelings, and is a potent excitatory amino acid agonist.

Both muscimol and ibotenic acid pass the blood-brain barrier better than GABA or glutamic acid.

Ibotenic acid is a powerful neurotoxicant and has been used as a potent brain-lesioning agent. When injected directly into the brains of mice, rats, or monkeys, it causes profound destruction of basal forebrain cholinergic neurons.

Ibotenic acid or (S)-2-amino-2-(3-hydroxyisoxazol-5-yl)acetic acid, also referred to as ibotenate, is a chemical compound and psychoactive drug which occurs naturally in Amanita muscaria and related species of mushrooms typically found in the temperate and boreal regions of the northern hemisphere.

Muscimol is one of the psychoactive compounds responsible for the effects of Amanita muscaria intoxication. Ibotenic acid, a neurotoxic secondary metabolite of Amanita muscaria, serves as a prodrug to muscimol when the mushroom is ingested or dried, converting to muscimol via decarboxylation.

Amanita muscaria
Ibotenic acid or (S)-2-amino-2-(3-hydroxyisoxazol-5-yl)acetic acid, also referred to as ibotenate, is a chemical compound and psychoactive drug which occurs naturally in Amanita muscaria and related species of mushrooms typically found in the temperate and boreal regions of the northern hemisphere.

Symptoms associated with ibotenic acid are usually onset within 30–60 minutes and include a range of nervous system effects. The most common symptoms include nausea, vomiting, and drowsiness.

The effects of the muscimol begin 30–120 minutes after consumption and last for 5–10 hours. These include euphoria, dream-like (lucid) state of mind, out-of-body experiences and synesthesia. Negative effects include mild to moderate nausea, stomach discomfort, increased salivation and muscle twitching or tremors.

It appears that the highest concentration is in the yellow tissue of the cap immediately below the skin. The most important active substance thus far isolated with regard to concentration is ibotenic acid.

Mechanism of action. The binding of ibotenic acid allows excess Ca 2+ into the system which results in neuronal cell death or apoptosis. Ca 2+ also activates CaM-KII or Ca 2+ /Calmodulin Kinase which phosphorylates multiple enzymes. The activated enzymes then begin producing reactive oxygen species which damages surrounding tissue.

The binding of ibotenic acid allows excess Ca 2+ into the system which results in neuronal cell death. Ca 2+ also activates CaM-KII or Ca 2+ /Calmodulin Kinase which phosphorylates multiple enzymes. The activated enzymes then begin producing reactive oxygen species which damages surrounding tissue.

Ibotenic acid used for the lesioning of rat’s brains is kept frozen in a phosphate-buffered saline solution at a pH of 7.4, and can be kept for up to a year with no loss in toxicity. Injection of .05-.1 microliters of Ibotenic acid into the hippocampus at a rate of .1 microliter/min resulted in semi-selective lesioning.

Gastrointestinal discomfort is uncommon and neurologic and psychotropic effects dominate; inebriation, euphoria alternating with anxiety, confusion, illusions, delusions, hallucinations, agitation, and violent behavior are also common. More uncommon symptoms are myoclonic jerks, muscle fasciculation and convulsions.