OA and TA can act both inside and outside of the nervous system, functioning as either a neurotransmitter or a neurohormone in insects Cole 2005. Thus, we explored whether the sugar response phenotype of tßh mutants was a result of alterations in neurons inside or outside of the brain or in non-neuronal cells. To this end, we expressed tßh in tßhnM18 mutant males using different GAL4-lines. We found a significant increase in sugar response compared to the respective mutant control when we used the ubiquitous Actin-promoter to drive Gal4 in all cells, the pan-neuronal nSyb-promoter, or the non-neuronal Tdc1-GAL4 driver (Fig. 6). In contrast, tßh expression in subsets of OA/TA-neurons, using either Tdc2- or NP7088-GAL4 did not significantly affect the mutants’ response (Fig. 6), in contrast to a previous report (NP7088-Gal4, Scheiner 2014). These last two results also show that the UAS construct alone is not sufficient to bring a rescue. These results indicate that tßh expression induced in neurons in the central nervous system or in non-neuronal cells, respectively, is sufficient to enhance the sugar responsiveness of tßhnM18 mutant flies.