Skip to end of metadata
Go to start of metadata


Author(s)

Year

Title

Publication Information

Link

Johnson, P.M. and Kenney, P.J.

2010

Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats

Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats

Nature Neuroscience 13(5): 635-641

PDF

Abstract: We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.

Introduction

1. Scientific Question
Johnson and Kenny question how down-regulation of dopamine D2 receptors (D2Rs) controls weight gain, reward thresholds, and the behavioral response to an adverse conditioned stimulus while feeding in order to better understand addiction-like compulsive feeding.

2. Main Hypothesis
The researchers explore two main hypotheses: (1) overconsumption of a palatable cafeteria diet reduces striatal D2R density and contributes to the development of addition-like hypo-sensitivity to rewards and (2) rats with knocked-down D2Rs given access to the cafeteria diet display addiction-like behavior similar to that seen in rats given cocaine or heroin; they continue eating despite punishment.

3. Methods

a. Brain Stimulation Reward
b. Surgical methods
c. Viral packaging and delivery
d. Cue-induced suppression of feeding behaviors
e. Immunoblotting

4. Conclusion

Click here to follow a detailed figure-by-figure annotation of this paper: Figure No.1 Weight gain and reward dysfunction in rats with extended access to a cafeteria diet


Return to the project home page Neural Reward and Addiction-like Compulsive Eating

  • No labels