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Octopamine mediates starvation-induced hyperactivity in adult Drosophila
Author(s) -
Zhe Yang,
Yue Yu,
Vivian Zhang,
Yinjun Tian,
Wei Qi,
Liming Wang
Publication year - 2015
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1417838112
Subject(s) - octopamine (neurotransmitter) , starvation , drosophila melanogaster , mushroom bodies , biology , foraging , energy homeostasis , insect , neural substrate , neuroscience , microbiology and biotechnology , feeding behavior , food intake , norepinephrine , drosophila (subgenus) , endocrinology , biochemistry , dopamine , ecology , serotonin , gene , receptor , obesity , cognition
Starved animals often exhibit elevated locomotion, which has been speculated to partly resemble foraging behavior and facilitate food acquisition and energy intake. Despite its importance, the neural mechanism underlying this behavior remains unknown in any species. In this study we confirmed and extended previous findings that starvation induced locomotor activity in adult fruit flies Drosophila melanogaster. We also showed that starvation-induced hyperactivity was directed toward the localization and acquisition of food sources, because it could be suppressed upon the detection of food cues via both central nutrient-sensing and peripheral sweet-sensing mechanisms, via induction of food ingestion. We further found that octopamine, the insect counterpart of vertebrate norepinephrine, as well as the neurons expressing octopamine, were both necessary and sufficient for starvation-induced hyperactivity. Octopamine was not required for starvation-induced changes in feeding behaviors, suggesting independent regulations of energy intake behaviors upon starvation. Taken together, our results establish a quantitative behavioral paradigm to investigate the regulation of energy homeostasis by the CNS and identify a conserved neural substrate that links organismal metabolic state to a specific behavioral output.

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