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A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder
Published on: June 18, 2018
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PPARγ agonism attenuates cocaine cue reactivity
William R Miller1,2,3, Robert G Fox2,4, Sonja J Stutz2,4
1Department of Neurology, Galveston, TX, USA.
Addiction Biology
|November 19, 2016
Summary
PPARγ agonism can help prevent cocaine relapse by reducing cue reactivity in rats. This approach may be a viable strategy for maintaining abstinence in individuals with cocaine use disorder.
Area of Science:
- Neuroscience
- Pharmacology
- Addiction Research
Background:
- Cocaine use disorder is a chronic relapsing condition.
- Exposure to drug-associated cues triggers craving and relapse in humans and animal models.
- Cue reactivity is a key factor in cocaine relapse prediction.
Purpose of the Study:
- To investigate the potential of PPARγ agonism as a relapse prevention strategy for cocaine use disorder.
- To assess the effect of PPARγ agonism on cue-induced cocaine-seeking behavior and associated neural mechanisms.
Main Methods:
- Sprague Dawley rats underwent cocaine self-administration followed by an abstinence period.
- Cue-reactivity tests were performed using previously active levers.
- PPARγ agonist and antagonist (GW9662) were administered.
- Nuclear ERK activity in the medial prefrontal cortex and hippocampus was measured.
Main Results:
- PPARγ agonism significantly reduced lever pressing during cue-reactivity tests.
- The PPARγ antagonist GW9662 reversed the effects of PPARγ agonism.
- PPARγ agonism normalized nuclear ERK activity in the medial prefrontal cortex and hippocampus, an effect reversed by GW9662.
Conclusions:
- PPARγ agonism demonstrates potential as a relapse prevention strategy for cocaine use disorder.
- Targeting PPARγ may help maintain abstinence by mitigating cue-induced cocaine-seeking behavior.
- Modulation of ERK activity in key brain regions is a potential mechanism underlying PPARγ's effects.
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