The FMRFamide-Gated Sodium Channel’s Effects on the EPSP Amplitude at the Neuromuscular Junction are Inconclusive

Abstract

Within the nervous system, neurons communicate at synapses via neurotransmitters transported between neurons until reaching the postsynaptic cell. They then bind to and activate specific proteins in the postsynaptic cell. Ion channels in the postsynaptic cell open and allow an influx of positive ions, depolarizing the cell, leading to an EPSP (Excitatory Postsynaptic Potential). FaNaC is a sodium-gated ion channel found in crayfish muscle cells that is activated by FMRFamide peptides. Since FaNaC allows positive ions into the postsynaptic cell, we sought to understand how it alters the strength of an EPSP by isolating the effects of FaNaC alone. We used NF1, a FMRFamide, to activate FaNaC. Additionally, we used a known FaNaC inhibitor, Amiloride, to see how EPSPs changed when FaNaC was not active. Protein kinases have also been implicated in the response to FMRFamide, so we utilized Staurosporine, a protein kinase inhibitor to isolate FaNaC and better understand its involvement in synaptic transmission. Our research potentially indicates that FaNaC decreases EPSP amplitude, but due to control discrepancies, it requires further research.