Nitric Oxide Mediates the Effect of DF₂ on EPSP Amplitude

Abstract

This experiment looked at the role of nitric oxide in the mechanism by which the peptide DF₂ increases neurotransmitter release at the crayfish neuromuscular junction. We hypothesized that if DF₂ increases neurotransmitter release through a pathway involving nitric oxide as a retrograde signal, then when L-NAME, an inhibitor of nitric oxide synthesis, was applied, DF₂ will not increase neurotransmitter release. To test this we exposed crayfish superficial dorsal extensor muscles to DF₂, which was amplified with IBMX. We then submerged the preparation into saline solution that contained DF₂, IBMX, and L-NAME. Neurotransmitter release was measured by the amplitude of EPSP traces recorded from the postsynaptic muscle cells via intracellular recording. Our data shows an increase in neurotransmitter release after exposure to DF₂ and IBMX, as well as a decrease in neurotransmitter release after the addition of L-NAME, a trend that supports our hypothesis. Further testing is needed to draw conclusions about our hypothesis.