DHA but not EPA, enhances sound induced escape behavior and Mauthner cells activity in Sparus aurata

- Escape swimming to sound is reduced in n − 3 HUFA deficient fish.
- n − 3 HUFA affects the increased immunofluorescence of ChAT in Mauthner cells.
- Dietary n − 3 HUFA deficiency reduces neural tissue contents of these fatty acids.
- Mauthner cells in n − 3 HUFA-deficient fish have lower acetylcholine production as measured by ChAT immunofluorescence.

Dietary omega − 3 long chain polyunsaturated fatty acids (n − 3 LCPUFA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have a marked effect on fish behavior. There is limited information on the mechanisms involved in this effect and its relation to neuron development and functioning. Deficiency of n − 3 LCPUFA reduces fish escape swimming. Mauthner cells (M-cell) are neurons responsible for initiating an escape response. The aim was to compare the effect of dietary DHA and EPA on escape behavior and neuronal activity of sea bream larvae. We studied burst swimming speed as a measure of behavior. M-cell activity was studied by ChAT immuno-fluorescence. Feeding the lowest n − 3 LCPUFA levels a lower burst swimming speed. Increase in dietary EPA did not significantly improve escape response. Elevation of dietary DHA was correlated with a higher burst speed denoting the importance of this nutrient for escape swimming. Incorporation of DHA into larval tissues was proportional to DHA dietary levels and significantly correlated with burst speed. In addition, a higher immunoreactivity to ChAT, associated to a higher neural activity, was found in M-cell of larvae fed higher dietary DHA contents. These results show first evidence of n − 3 LCPUFA on fish neuronal activity and their implications in behavior, denoting that DHA boosts escape swimming and this effect is at least partly mediated by the increase in neural activity of M-cell.