conformations which are shown superimposed in this image. Because of this similarity,<unk>  binds to certain GABA-receptors.<unk>  is a potent GABAA agonist, activating the receptor for the brain's principal inhibitory neurotransmitter, GABA.<unk>  binds to the same site on the GABAA receptor complex as GABA itself, as opposed to other GABAergic drugs such as barbiturates and benzodiazepines which bind to separate regulatory sites. GABAA receptors are widely distributed in the brain, and so when<unk>  is administered, it alters neuronal activity in multiple regions including the cerebral cortex, hippocampus, and cerebellum. While<unk>  is normally thought of as a selective GABAA agonist with exceptionally high affinity to GABAA-delta receptors, it is also a partial agonist at the GABAA-rho receptor, and so its range of effects results from a combined action on more than one GABAA receptor subtype. The psychoactive dose of<unk>  is around 10–15 mg for a normal person. A Guide to British Psilocybin Mushrooms by Richard Cooper published in 1977 recommends a smaller dose, 8.5 mg, and suggests that it is possible for this amount to be present in as little as 1 g of dried A. muscaria but this is not consistent with most other reports which suggest 5–10 g is necessary. A correct dose may be difficult to determine because potency varies dramatically from one mushroom to the next. When consumed, a substantial percentage of<unk>  goes un-metabolized and thus excreted in urine, a phenomenon exploited by practitioners of the traditional entheogenic use of Amanita muscaria. In patients with Huntington's disease and chronic schizophrenia, oral doses of<unk>  have been found to cause a rise of both prolactin and growth hormone. During a test involving rabbits connected to an EEG,<unk>  presented with a distinctly synchronized EEG tracing. This is substantially different from serotonergic psychedelics, with which brainwave patterns generally show a desynchronization. In higher doses (2 mg/kg via IV), the EEG will show characteristic spikes. Effects The effects of the<unk>  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. In large doses strong dissociation or delirium may be felt. Many of<unk> 's effects are consistent with its pharmacology as a GABAA receptor agonist, presenting many depressant or sedative-hypnotic effects. Atypical of the effect profile of sedative drugs generally however,<unk> , like Z-drugs, can cause hallucinogenic changes in perception. The hallucinogenic effect produced by<unk>  is most closely comparable to the hallucinogenic side effects produced by some other GABAergic drugs such as zolpidem.
Muscimol
Acetylcholine
Lysergic acid diethylamide
Anatoxin-a
Thiotepa
Opioid peptide
Neuropil
Procaine