Abstract: Objective: Changes in the behavior and motility of Littorina molluscs caused by parasitic trematode infection have been known to researchers for over 40 years. However, the mechanisms underlying these effects of trematodes on mollusc physiology remain unclear. In this study, we investigated tissue content of monoamines, which are involved in regulating locomotion, and the activity of acetylcholinesterase, an enzyme involved in neuromuscular signal transduction. Methods: Healthy and infected (with Microhallus pygmaeus or M. piriformes) molluscs Littorina saxatilis and L. obtusata were studied. We evaluated dopamine, serotonin, 5-hydroxyindoleacetic acid, and norepinephrine tissue content using high-performance liquid chromatography with electrochemical detection, and measured acetylcholinesterase activity according to the Ellman method in the tissues of trematode-infected molluscs in comparison with uninfected individuals. Results and Discussion: Trematode infection caused an increase in norepinephrine content and serotonin turnover in L. obtusata molluscs, while these effects were absent in L. saxatilis. No changes in acetylcholinesterase activity caused by trematode infection were observed for either of the species. We discuss the potential physiological systems impacted by parasitism in L. obtusata, and propose explanations for species-specific variation in host-parasite interactions. Conclusions: Despite their phylogenetic and ecological proximity, L. saxatilis and L. obtusata exhibit divergent neurophysiological outcomes following infection with Microphallus trematodes. These preliminary results suggest host-specific impacts on mobility control and underscore the relevance of neurotransmitter analysis in understanding trematode-driven behavioral alterations.