Dopamine receptor 1 neurons in the dorsal striatum regulate food anticipatory circadian activity rhythms in mice
- Creators
- Gallardo, Christian M.
- Darvas, Martin
- Oviatt, Mia
- Chang, Chris H.
- Michalik, Mateusz
- Huddy, Timothy F.
- Meyer, Emily
- Shuster, Scott A.
- Aguayo, Antonio
- Hill, Elizabeth M.
- Kiani, Kaun
- Ikpeazu, Jonathan
- Martinez, Johan S.
- Purpura, Mari
- Smit, Andrea N.
- Patton, Danica
- Mistlberger, Ralph E.
- Palmiter, Richard D.
- Steele, Andrew D.
Abstract
Daily rhythms of food anticipatory activity (FAA) are regulated independently of the suprachiasmatic nucleus, which mediates entrainment of rhythms to light, but the neural circuits that establish FAA remain elusive. Here we show that mice lacking the dopamine D1 receptor (D1R KO mice), manifest greatly reduced FAA, whereas mice lacking the dopamine D2 receptor have normal FAA. To determine where dopamine exerts its effect, we limited expression of dopamine signaling to the dorsal striatum of dopamine-deficient mice; these mice developed FAA. Within the dorsal striatum, the daily rhythm of clock gene per2 expression was markedly suppressed in D1R KO mice. Pharmacological activation of D1R at the same time daily was sufficient to establish anticipatory activity in wild-type mice. These results demonstrate that dopamine signaling to D1R in the dorsal striatum plays an important role in manifestation of FAA, possibly by synchronizing circadian oscillators that modulate motivational processes and behavioral output.
Additional Information
© 2014, Gallardo et al. Received June 25, 2014. Accepted September 10, 2014. Published September 12, 2014. This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited. This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited. Funding was provided by the Broad Fellows Program in Brain Circuitry at Caltech, an Ellison Medical Foundation New Scholar Award to ADS, a Grants Program in Eating Disorders Research from the Klarman Family Foundation to ADS, a Claremont McKenna Interdisciplinary Science Scholarship to CHC, a HHMI summer fellowship to EM, an Natural Sciences and Engineering Research Council (Canada) operating grant to REM, and NSERC scholarships to MM and DFP, and a National Institutes of Health Center Grant P50 NS062684. We are grateful to members of the Palmiter laboratory and to Henry Lester, David Anderson, and Christof Koch (Caltech) for helpful advice. We are also grateful to Teagan Wall for assistance with Minimitter implantation surgery.Attached Files
Published - elife-03781-v2.pdf
Accepted Version - eLife_03781_full_acceptedversion.pdf
Supplemental Material - 12_eLife_03781_DC1_elife03781_Supplemental_files.zip
Supplemental Material - elife-03781-figures-v2.pdf
Files
Additional details
- PMCID
- PMC4196120
- Eprint ID
- 50354
- Resolver ID
- CaltechAUTHORS:20141013-130954074
- Caltech Broad Fellows Program in Brain Circuitry
- Ellison Medical Foundation
- Klarman Family Foundation Program in Eating Disorders Research
- Claremont-McKenna Interdisciplinary Science Scholarship
- Howard Hughes Medical Institute (HHMI)
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- P50 NS062684
- NIH
- Created
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2014-10-13Created from EPrint's datestamp field
- Updated
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2023-09-26Created from EPrint's last_modified field