Published April 1, 2010 | Version Published
Journal Article Open

A Pair of Dopamine Neurons Target the D1-Like Dopamine Receptor DopR in the Central Complex to Promote Ethanol-Stimulated Locomotion in Drosophila

  • 1. ROR icon University of California, San Francisco
  • 2. ROR icon University of Virginia
  • 3. ROR icon California Institute of Technology

Abstract

Dopamine is a mediator of the stimulant properties of drugs of abuse, including ethanol, in mammals and in the fruit fly Drosophila. The neural substrates for the stimulant actions of ethanol in flies are not known. We show that a subset of dopamine neurons and their targets, through the action of the D1-like dopamine receptor DopR, promote locomotor activation in response to acute ethanol exposure. A bilateral pair of dopaminergic neurons in the fly brain mediates the enhanced locomotor activity induced by ethanol exposure, and promotes locomotion when directly activated. These neurons project to the central complex ellipsoid body, a structure implicated in regulating motor behaviors. Ellipsoid body neurons are required for ethanol-induced locomotor activity and they express DopR. Elimination of DopR blunts the locomotor activating effects of ethanol, and this behavior can be restored by selective expression of DopR in the ellipsoid body. These data tie the activity of defined dopamine neurons to D1-like DopR-expressing neurons to form a neural circuit that governs acute responding to ethanol.

Additional Information

© 2010 Kong et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Received January 27, 2010; Accepted March 11, 2010. Published online 2010 April 1. Funding for this research was provided by United States National Institutes of Health grant AA014594-04 (FWW), GM27318 (JH), DA19573 (UH), and GM081863-03 (RJB). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Editor: Mark A. Frye, UCLA, United States of America. We thank Karen Berger for the inebriometer tolerance assay, Viktor Kharazia, Elizabeth Marin, and Liqun Luo for assistance with fly brain imaging, Willa Abrone for technical assistance, David Anderson for support and advice, Bing Ye and Steve Stowers for reagents, the Bloomington and Harvard Drosophila stock centers for strains. Author Contributions: Conceived and designed the experiments: ECK KW UH JH FW. Performed the experiments: ECK KW HL NM MRS FW. Analyzed the data: ECK HL RJB FW. Contributed reagents/materials/analysis tools: ECK TL RJB. Wrote the paper: FW.

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Additional details

Identifiers

PMCID
PMC2848596
Eprint ID
18633
Resolver ID
CaltechAUTHORS:20100610-085851595

Funding

NIH
AA014594-04
NIH
GM27318
NIH
DA19573
NIH
GM081863-03

Dates

Created
2010-07-15
Created from EPrint's datestamp field
Updated
2021-11-08
Created from EPrint's last_modified field