Exogenous AMP decreases EPP amplitude at the frog neuromuscular junction

Abstract

The communication between the motor nerve and the skeletal muscle can be disrupted by repetitive stimulation of the nerve, a phenomenon known as presynaptic depression. This depression is caused by the co-release of ATP with the neurotransmitter acetylcholine (ACh) during nerve stimulation, as the ATP and its hydrolysis product inhibit further release of ACh. Using the sartorius muscle and vagus nerve of Rana pipiens pipiens, we used intracellular recording techniques to test the effects of exogenous AMP on neurotransmitter release. We found that, like ATP and adenosine, AMP significantly decreases EPP amplitude. Therefore, we believe that AMP is either: a) converting to ATP or adenosine and then acting through these pathways or b) binding to unidentified AMP-specific receptors to cause a decrease in ACh release.