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Published November 25, 2009 | Accepted Version + Supplemental Material
Journal Article Open

Two Different Forms of Arousal in Drosophila Are Oppositely Regulated by the Dopamine D1 Receptor Ortholog DopR via Distinct Neural Circuits

Abstract

Arousal is fundamental to many behaviors, but whether it is unitary or whether there are different types of behavior-specific arousal has not been clear. In Drosophila, dopamine promotes sleep-wake arousal. However, there is conflicting evidence regarding its influence on environmentally stimulated arousal. Here we show that loss-of-function mutations in the D1 dopamine receptor DopR enhance repetitive startle-induced arousal while decreasing sleep-wake arousal (i.e., increasing sleep). These two types of arousal are also inversely influenced by cocaine, whose effects in each case are opposite to, and abrogated by, the DopR mutation. Selective restoration of DopR function in the central complex rescues the enhanced stimulated arousal but not the increased sleep phenotype of DopR mutants. These data provide evidence for at least two different forms of arousal, which are independently regulated by dopamine in opposite directions, via distinct neural circuits.

Additional Information

© 2009 Elsevier Inc. Under an Elsevier user license. Accepted 16 September 2009. Published: November 25, 2009. Available online 25 November 2009. We thank Ulrike Heberlein for sharing unpublished data and providing the manifold for the puff-o-mat, Martin Heisenberg and members of the Anderson lab for helpful comments on the manuscript, Eric Hoopfer for help with imaging, Michael Reiser for contributions to software development, Mary Wahl for assistance with screening, Tim Tayler for sharing Gal4 stocks prior to publication, Shilpa Jeeda for maintenance of stocks, Gaby Mosconi for lab management, and Gina Mancuso for Administrative Support. Fly stocks were obtained from the Bloomington and Harvard stock centers and also generously provided by Doug Armstrong. T.J.L. was a fellow of the Jane Coffin Childs Foundation and H.D. a fellow of the Alexander von Humboldt Association. Supported in part by an NSF FIBR grant to D.J.A., P.P., and Michael Dickinson. D.J.A. is an Investigator of the Howard Hughes Medical Institute. This paper is dedicated to the late Seymour Benzer.

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Supplemental Material - mmc1.pdf

Supplemental Material - mmc2.mov

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