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Shiny rhomboid leaflets

Colorless, shining, prismatic crystals or white or nearly white microcrystalline powder

1 g in 350 ml water

1 g in 5 ml boiling water (approx)

1 g in 13.5 ml 95% ethanol

1 g in 3 ml boiling alcohol (approx)

For more Solubility (Complete) data for PICROTOXIN (7 total), please visit the HSDB record page.

397 °F (EPA, 1998)

203 °C

Cocculus appears as a poisonous berry, the dried fruit of Anamirta cocculus L. Contains several substances including about one percent picrotoxin. Pure picrotoxin occurs as shiny leaflets with an intensely bitter taste or as a microcrystalline powder. Very poisonous!. Used in medicine as a central nervous system stimulant and antidote for barbiturate poisoning. Not currently regarded as a useful therapeutic agent.

Danger

H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]

P264, P270, P301+P316, P321, P330, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 43 reports by companies from 1 notifications to the ECHA C&L Inventory.

Cocculus

Marine pollutant

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Picrotoxin is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 500/10,000 lbs.

Picrotoxin is a toxin obtained from the seeds of the shrub <i>Anamirta cocculus</i>. It is used as a central nervous system stimulant, antidote, convulsant, and GABA (gamma aminobutyric acid) antagonist. It is a noncompetitive antagonist at GABA_A receptors and thus a convulsant. Picrotoxin blocks the GABA_Activated chloride ionophore. Although it is most often used as a research tool, it has been used as a CNS stimulant and an antidote in poisoning by CNS depressants, especially barbiturates.

Picrotoxin antagonizes the GABA_A receptor channel directly, which is a ligand-gated ion channel concerned chiefly with the passing of chloride ions across the cell membrane. Therefore picrotoxin prevents Cl^- channel permeability and thus promtes an inhibitory influence on the target neuron. Picrotoxin reduces conductance through the channel by reducing not only the opening frequency but also the mean open time. Picrotoxin also antagonizes GABA_C receptors (also called GABA_A-rho receptors) but the result of this action is not known. The GABA_C receptor is also linked to chloride channels, with distinct physiological and pharmacological properties. In contrast to the fast and transient responses elicited from GABA_A receptors, GABA_C receptors mediate slow and sustained responses.

In mammals it has been shown that picrotoxin blocks presynaptic inhibition and strychnine-resistant postsynaptic inhibition in the central nervous system. Picrotoxin selectively antagonizes the effects of the predominant inhibitory transmitter, gamma-aminobutyric (GABA), at all levels of the central nervous system. Current information indicates that GABA receptors are coupled to ionophores that permit the influx of chloride with resultant hyperpolarization of neuronal membranes. Picrotoxin antagonizes the effects of GABA, perhaps by interacting with sites closely associated with the ionophore. A similarly acting convulsant drug, bicuculline, interacts directly with the GABA receptor and is therefore a true antagonist. Both drugs produce convulsions by blocking the inhibitory pathways mediated by GABA. The relative importance of blockade of presynaptic or postsynaptic inhibition for their convulsant activity is unknown.