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ABSTRACT Snails belonging to the genusBiomphalariaserve as obligatory intermediate hosts for the trematodeSchistosoma mansoni, the causative agent for the most widespread form of schistosomiasis. The simpler nervous systems of gastropod molluscs, such asBiomphalaria, provide advantageous models for investigating neural responses to infection at the cellular and network levels. The present study examined neuropeptides related to cholecystokinin (CCK), a major multifunctional regulator of central nervous system (CNS) function in mammals. A neural transcriptome generated from the CNS ofBiomphalaria alexandrinaincluded a transcript encoding two CCK‐related peptides, designatedBalex‐CCK1 (pEGEWSYDY_(SO3H)GLGGGRF‐NH₂) andBalex‐CCK2 (NYGDY_(SO3H)GIGGGRF‐NH₂). Peptide expression was examined inBiomphalaria glabrataat the mRNA level using the hybridization chain reaction (HCR) protocol and at the protein level using an antibody againstBalex‐CCK1. Expression was detected in 60–70 neurons distributed throughout the CNS, as well as in profuse fiber systems connecting the ganglia and projecting to the periphery. CCK‐like immunoreactive (CCK_li) fibers were also observed on organs associated with the cardiorespiratory (nephridium, mantle, gill) and male reproductive systems. A comparison of mRNA and peptide localization suggested that CCK expression could be regulated at the level of translation. A potential role of these peptides in mediating responses to infection by larval schistosomes is discussed. 

Neuronal signals mediated by the biogenic amine serotonin underlie critical survival strategies across the animal kingdom. This investigation identified a group of serotonergic cells in the panpulmonate snail Biomphalaria glabrata that appear to be homologous to neurons that mediate withdrawal responses in other gastropod taxa. It is proposed that an ancient withdrawal circuit has been highly conserved in three major gastropod lineages. 

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 genus Biomphalaria to 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 the Biomphalaria intermediate host could lead to novel strategies for parasite or snail control. This study examined a Biomphalaria glabrata neural channel that is gated by the neuropeptide FMRF-NH 2 . The Biomphalaria glabrata FMRF-NH 2 gated sodium channel ( Bgl- FaNaC) amino acid sequence was highly conserved with FaNaCs found in related gastropods, especially the planorbid Planorbella trivolvis (91% sequence identity). In common with the P . trivolvis FaNaC, the B . glabrata channel exhibited a low affinity (EC 50 : 3 x 10 −4 M) and high specificity for the FMRF-NH 2 agonist. Its expression in the central nervous system, detected with immunohistochemistry and in situ hybridization, was widespread, with the protein localized mainly to neuronal fibers and the mRNA confined to cell bodies. Colocalization of the Bgl- FaNaC message with its FMRF-NH 2 agonist 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) by S . mansoni . Increased expression of the transcript encoding the FMRF-NH 2 agonist at 35 dpi was proposed to reflect a compensatory response to decreased receptor levels. Altered FMRF-NH 2 signaling could be vital for parasite proliferation in its intermediate host and may therefore present innovative opportunities for snail control.