The larval flatworm Microphallus papillorobustus encysts in the protocerebrum of its intermediate host, Gammarus insensibilis, and changes the gammarid's responses to mechanical and photic stimuli. The resulting aberrant escape behaviour renders infected gammarids more susceptible to predation by birds, the definitive hosts of the parasite. We used immunocytochemical methods to explore the mechanisms underlying these subtle behavioural modifications. Whole mounts of gammarid brains were labelled with fluorescent anti-serotonin and anti-synapsin antibodies and viewed using confocal microscopy. Two types of change were observed in infected brains: the intensity of the serotonergic label was altered in specific regions of the brain, and the architecture of some serotonergic tracts and neurons was affected. A morphometric analysis of the distribution of the label showed that serotonergic immunoreactivity was decreased significantly (by 62%) in the optic neuropils, but not in the olfactory lobes, in the presence of the parasite. In addition, the optic tracts and the tritocerebral giant neurons were stunted in parasitized individuals. Published evidence demonstrates changes in serotonin levels in hosts ranging from crustaceans to mammals infected by parasites as diverse as protozoans and helminths. The present study suggests that the degeneration of discrete sets of serotonergic neurons might underlie the serotonergic imbalance and thus contribute to host manipulation.