Abstract
Abstract Threespine sticklebacks Gasterosteus aculeatus infected with the tapeworm Schistocephalus solidus display impairments in their anti‐predator responses. They also have increased expression of the gene encoding the IMPase 1 enzyme in their brains, which is part of a key step in myo‐inositol synthesis. IMPase 1 and myo‐inositol levels are the targets of lithium treatment in patients with bipolar disorder. Although promising candidates, we do not know if IMPase 1 and myo‐inositol are directly implicated in the changes in risky behaviours measured in Schistocephalus‐infected fish. Understanding the molecular mechanisms directly or indirectly involved in these behavioural alterations is crucial to understand the evolution of host–parasite interactions. Here, we increased myo‐inositol levels of uninfected fish and inhibited IMPase 1 activity in infected fish to test the prediction that it would decrease and increase their anti‐predator behaviour respectively. We found that uninfected fish with increased myo‐inositol levels (by injecting exogenous myo‐inositol or by inducing endogenous production using an osmotic challenge) did not decrease their anti‐predator responses. However, infected fish treated with lithium chloride had some of their anti‐predator behaviours restored, but not all. They spent less time swimming close to the surface, showed lowered activity, had a higher latency to feed in a novel environment and spent more time frozen after a predator attack. Our results suggest that the target of lithium treatment is implicated in the risky behaviours of infected fish and supports the idea that the parasite‐associated alteration in behaviour has a multifactorial nature. Read the free Plain Language Summary for this article on the Journal blog.
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