Apamin blocks certain neurotransmitter-induced increases in potassium permeability

Abstract

Apamin¹ is a neurotoxic polypeptide of known structure^2,3 isolated from bee venom. Shuba and coworkers^4,5 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 proposed⁶ that ATP is the neurotransmitter involved in the latter response, Vladimirova and Shuba⁴ 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.