Muscimol

Direct GABA-A agonist from Amanita muscaria — rare mechanism (most "GABAergics" are PAMs), but the actual experience is sedation + dissociation + delirium with hours-long impairment, not anxiolysis you'd want daily. FDA flagged it as an unapproved food additive in Dec 2024 after hundreds of poison-control calls and Diamond Shruumz outbreak (180 illnesses, 73 hospitalizations, 3 suspected deaths). Skip — Dylan already has cleaner sleep/anxiety levers.

Muscimol is the decarboxylated active form of ibotenic acid (drying/cooking Amanita muscaria converts most ibotenic acid → muscimol; raw mushroom is significantly more toxic via NMDA excitotoxicity from undecarboxylated ibotenic acid).

Primary action: Direct orthosteric agonist at GABA-A receptors — binds the same site GABA itself binds, opening the chloride channel and producing inhibitory hyperpolarization. This is mechanistically distinct from:

• Benzodiazepines / Z-drugs / barbiturates — positive allosteric modulators (PAMs), enhance GABA's effect but don't open channels alone
• Theanine, taurine, glycine, "GABA supplements" — indirect / mixed / barely cross BBB / weak modulators
• Phenibut, baclofen — GABA-B agonists, completely different receptor family

Subunit selectivity: Strong preference for δ-subunit-containing extrasynaptic GABA-A receptors (high tonic inhibition territory) over the synaptic γ2-containing receptors that benzos prefer. This is why the experience differs from a benzo high — more tonic global inhibition, more dissociation, less clean anxiolysis.

Secondary: Partial agonist at GABA-A-ρ (formerly "GABA-C"); weak GABA reuptake substrate. Inactive at GABA-B.

BBB: Crosses readily (unlike GABA itself). Centrally active orally.