Journal article
Melanocortin 4 receptor signaling in dopamine 1 receptor neurons is required for procedural memory learning
Physiology & behavior, Vol.106(2), pp.201-210
05/15/2012
DOI: 10.1016/j.physbeh.2012.01.025
PMCID: PMC3314089
PMID: 22342812
Abstract
It is now widely recognized that exposure to palatable foods engages reward circuits that promote over-eating and facilitate the development of obesity. While the melanocortin 4 receptor (MC4R) has previously been shown to regulate food intake and energy expenditure, little is known about its role in food reward. We demonstrate that MC4R is co-expressed with the dopamine 1 receptor (D1R) in the ventral striatum. While MC4R-null mice are hyperphagic and obese, they exhibit impairments in acquisition of operant responding for a high fat reinforcement. Restoration of MC4R signaling in D1R neurons normalizes procedural learning without affecting motivation to obtain high fat diet. MC4R signaling in D1R neurons is also required for learning in a non-food-reinforced version of the cued water maze. Finally, MC4R signaling in neostriatal slices increases phosphorylation of the Thr34 residue of DARPP-32, a protein phosphatase-1 inhibitor that regulates synaptic plasticity. These data identify a novel requirement for MC4R signaling in procedural memory learning.
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► The melanocortin 4 receptor (MC4R) is expressed in a dopamine 1 receptor neurons. ► MC4R signaling regulates acquisition of operant responding for palatable food. ► MC4R signaling is required for learning in a cued version of the water maze. ► DARPP-32, a regulator of synaptic plasticity, is phosphorylated after MC4R agonist.
Details
- Title: Subtitle
- Melanocortin 4 receptor signaling in dopamine 1 receptor neurons is required for procedural memory learning
- Creators
- Huxing Cui - Department of Internal Medicine (Division of Hypothalamic Research), University of Texas Southwestern Medical Center Dallas, Dallas, TX 75390-9127, United StatesBrittany L Mason - Department of Psychiatry, University of Texas Southwestern Medical Center Dallas, Dallas, TX 75390-9127, United StatesCharlotte Lee - Department of Internal Medicine (Division of Hypothalamic Research), University of Texas Southwestern Medical Center Dallas, Dallas, TX 75390-9127, United StatesAkinori Nishi - Kurume University School of Medicine, Department of Pharmacology, Kurume, Fukuoka, 830-0011, JapanJoel K Elmquist - Department of Internal Medicine (Division of Hypothalamic Research), University of Texas Southwestern Medical Center Dallas, Dallas, TX 75390-9127, United StatesMichael Lutter - Department of Psychiatry, University of Texas Southwestern Medical Center Dallas, Dallas, TX 75390-9127, United States
- Resource Type
- Journal article
- Publication Details
- Physiology & behavior, Vol.106(2), pp.201-210
- DOI
- 10.1016/j.physbeh.2012.01.025
- PMID
- 22342812
- PMCID
- PMC3314089
- NLM abbreviation
- Physiol Behav
- ISSN
- 0031-9384
- eISSN
- 1873-507X
- Publisher
- Elsevier Inc
- Grant note
- name: DK081185-01; name: DK081182-01; name: MH084058-01A1; name: Disease Oriented Clinical Scholars Program; name: NARSAD; name: JST; name: R01DK53301; name: RL1DK081185
- Language
- English
- Date published
- 05/15/2012
- Academic Unit
- Iowa Neuroscience Institute; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology
- Record Identifier
- 9984040321402771
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