FRMFamide Combined with IBMX Decreases EPSP Amplitude

Abstract

The aim of this experiment was to explore the effects of the neuropeptide FMRFamide (FMRFa) on the crayfish neuromuscular junction (CNJ). In previous experiments, DF₂, a FMRFa-like peptide, has been shown to increase neurotransmitter (NT) release at the CNJ. We hypothesized that, like DF₂, FMRFa would also potentiate the release of NT and thereby increase excitatory postsynaptic potential (EPSP) amplitude. We also hypothesized that IBMX, a phosphodiesterase inhibitor, would be needed to potentiate the excitatory effects of FMRFa, which it has been shown to do with DF₂. To test these hypotheses, we exposed the crayfish to both a high and low Ca²⁺ Ringers solution and to various treated solutions. The first treated solution contained just FMRFa, the second IBMX, and the third both FMRFa and IBMX. We then measured NT release by EPSP amplitudes, recorded from postsynaptic muscle cells via intracellular recording. Our data showed a trend that in both low and high Ca²⁺ Ringers solution, FMRFa did increase neurotransmitter release, supporting our first hypothesis. Our second hypothesis was rejected, for our data showed that in a FMRFa and IBMX treated solution average EPSP amplitude decreased.