The neglected tropical disease schistosomiasis impacts over 700 million people globally.Schistosoma mansoni, the trematode parasite that causes the most common type of schistosomiasis, requires planorbid pond snails of the genusBiomphalariato support its larval development and transformation to the cercarial form that can infect humans. A greater understanding of neural signaling systems that are specific to theBiomphalariaintermediate host could lead to novel strategies for parasite or snail control. This study examined aBiomphalaria glabrataneural channel that is gated by the neuropeptide FMRF-NH2. TheBiomphalaria glabrataFMRF-NH2gated sodium channel (Bgl-FaNaC) amino acid sequence was highly conserved with FaNaCs found in related gastropods, especially the planorbidPlanorbella trivolvis(91% sequence identity). In common with theP.trivolvisFaNaC, theB.glabratachannel exhibited a low affinity (EC50: 3 x 10−4M) and high specificity for the FMRF-NH2agonist. Its expression in the central nervous system, detected with immunohistochemistry andin situhybridization, was widespread, with the protein localized mainly to neuronal fibers and the mRNA confined to cell bodies. Colocalization of theBgl-FaNaC message with its FMRF-NH2agonist precursor occurred in some neurons associated with male mating behavior. At the mRNA level,Bgl-FaNaC expression was decreased at 20 and 35 days post infection (dpi) byS.mansoni. Increased expression of the transcript encoding the FMRF-NH2agonist at 35 dpi was proposed to reflect a compensatory response to decreased receptor levels. Altered FMRF-NH2signaling could be vital for parasite proliferation in its intermediate host and may therefore present innovative opportunities for snail control.