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Fat Preference: A Novel Model of Eating Behavior in Rats
Published on: June 27, 2014
Eating induced by perifornical cAMP is behaviorally selective and involves protein kinase activity
E R Gillard1, A M Khan, B Mouradi
1Department of Pharmacology, University of Alberta, Edmonton, Alberta, Canada T6G OK6.
The American Journal of Physiology
|August 4, 1998
Summary
Increasing cyclic AMP (cAMP) in the perifornical hypothalamus (PFH) triggers significant eating in rats. This effect is specific to the PFH and mediated by protein kinase A, highlighting cAMP
Area of Science:
- Neuroscience
- Molecular Biology
- Behavioral Science
Background:
- Endogenous cyclic AMP (cAMP) agents injected into the perifornical hypothalamus (PFH) stimulate eating.
- This suggests a critical role for PFH cAMP in regulating appetite and food intake.
Purpose of the Study:
- To investigate the role of cAMP in the PFH in controlling eating behavior.
- To determine if increased cAMP production in the PFH can selectively induce eating.
Main Methods:
- Bilateral microinjection of the adenylyl cyclase activator MPB forskolin into the PFH of satiated rats.
- Administration of an inactive analog (1, 9-dideoxyforskolin) and a protein kinase A inhibitor (H-89) to assess specificity.
- Observation and quantification of eating, gnawing, and drinking behaviors.
Main Results:
- MPB forskolin induced intense eating (15.7 +/- 2.3 g in 2 h) without affecting other behaviors.
- The inactive analog of forskolin did not elicit eating, confirming pharmacological specificity.
- The protein kinase A inhibitor H-89 reduced MPB forskolin-induced eating by up to 50%.
Conclusions:
- Increased cAMP production within the PFH is sufficient to selectively generate eating behavior.
- The effects are mediated through the activation of cAMP-dependent protein kinase.
- This research provides insight into the molecular mechanisms of appetite regulation in the brain.
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