Actions of Ptychodiscus brevis red tide toxin on metabolic and transmitter-releasing properties of synaptosomes.
A pure toxin isolated from Ptychodiscus brevis stimulated differential release of amino acid neurotransmitters from mammalian cortical synaptosomes together with loss of K+ content and respiratory stimulation at 40 ng/ml. The effect was blocked by tetrodotoxin and by verapamil, implicating Na+ channel activation and possibly Ca2+ influx as necessary for the response, although the response did not change upon omission of Ca2+. Verapamil was therefore likely to be acting as a Na+ channel blocker in this instance. The toxin at 40 ng/ml caused acetylcholine release from guinea pig ileum, which is consistent with the proposed depolarising action for the toxin.
D000109:Acetylcholine / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002540:Cerebral Cortex / Q000648:ultrastructure; D004141:Dinoflagellida; D005260:Female; D006168:Guinea Pigs; D007082:Ileum / Q000187:drug effects / Q000378:metabolism; D007473:Ion Channels / Q000187:drug effects; D008387:Marine Toxins / Q000494:pharmacology*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013574:Synaptosomes / Q000187:drug effects* / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D000596:Amino Acids; D007473:Ion Channels; D008387:Marine Toxins; D018377:Neurotransmitter Agents; D013779:Tetrodotoxin; D012964:Sodium; D014700:Verapamil; D000109:Acetylcholine