ATP depresses end-plate potential amplitude through nitric oxide independent pathways in the frog neuromuscular junction

Abstract

Given the similar depressive effects of ATP and nitric oxide on end-plate potential magnitude at the frog neuromuscular junction, it is reasonable to suspect that they may be acting via the same pathway. This investigation aimed to determine whether administration of N-v-Nitro-L-arginine-methyl-ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, could block the depressive effects of ATP. In our experiment, we measured EPP amplitudes in a nerve-muscle preparation exposed to L-NAME, to which ATP was added. ATP decreased EPP amplitude despite the blocked NO synthesis.