The FMRF-NH2Gated Sodium Channel ofBiomphalaria glabrata: Localization and Expression Following Infection bySchistosoma mansoni

Abstract

AbstractThe neglected tropical disease schistosomiasis impacts the lives of 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 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 characterized aBiomphalaria glabrataneural receptor that is gated by the molluscan 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. glabratareceptor exhibited a low affinity (EC50: 3 × 10−4M) and high specificity for the FMRF-NH2agonist. Its expression in the central nervous system, detected by immunohistochemistry andin situhybridization, was widespread, with the protein localized mainly to neuronal fibers and the mRNA confined to cell bodies. Colocalization was observed with the FMRF-NH2tetrapeptide precursor in some neurons associated with male mating behavior. At the mRNA level,Bgl-FaNaC expression in the visceral and left parietal ganglia decreased at 20 days post infection byS. mansoniand in the shedding phase. Altered FMRF-NH2signaling could be vital for parasite survival and proliferation in its snail intermediate host.