Apamin blocks certain neurotransmitter-induced increases in potassium permeability.
Apamin is a neurotoxic polypeptide of known structure isolated from bee venom. Shuba and coworkers have recently shown that it abolishes the hyperpolarising action of externally-applied ATP on visceral smooth muscle (guinea pig stomach and taenia coli) as well as the hyperpolarisation (inhibitory junction potential) that follows stimulation of the non-adrenergic inhibitory nerve supply to these tissues.  As it has been proposed that ATP is the neurotransmitter involved in the latter response, Vladimirova and Shuba tentatively concluded that apamin is a specific postsynaptic blocking agent of this non-adrenergic, possibly 'purinergic', inhibition. We have confirmed the important observation that nanomolar concentrations of apamin reduce inhibition by ATP and by non-adrenergic nerve stimulation, but further experiments suggest that, rather than acting as a specific blocker of ATP receptors, apamin inhibits the increase in potassium permeability caused by a number of agents, including ATP.
D000255:Adenosine Triphosphate / Q000037:antagonists & inhibitors; D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001514:Bee Venoms / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D006168:Guinea Pigs; D007422:Intestines / Q000187:drug effects; D007473:Ion Channels / Q000187:drug effects*; D008099:Liver / Q000187:drug effects; D011941:Receptors, Adrenergic / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D001514:Bee Venoms; D007473:Ion Channels; D011941:Receptors, Adrenergic; D001030:Apamin; D000255:Adenosine Triphosphate; D002118:Calcium