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. 2018 Jan 15;11:100. doi: 10.3389/fnsys.2017.00100

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Copyright © 2018 Damrau, Toshima, Tanimura, Brembs and Colomb.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Spatially controlled Tßh expression in tßh^nM18 mutant background. Ubiquitous (actin), pan-neuronal (nSyb) and non-neuronal TDC (Tdc1) drivers significantly increased sugar responsiveness. Neuronal TDC (tdc2) and OA (NP7088) specific drivers did not alter sugar responsiveness. Boxplots depict total number of proboscis extensions in hemizygous mutant males with or without a UAS-tßh construct, and heterozygous for the Gal4 driver. Numbers indicate sample sizes, asterisks denote significant difference between the mutant its respective rescue group (Wilcoxon rank sum test, Actin p = 0.01621, Tdc1 p = 0.02782, nSyb p = 0.01341).