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PPARγ agonism attenuates cocaine cue reactivity
Author(s) -
Miller William R,
Fox Robert G,
Stutz Sonja J,
Lane Scott D,
Denner Larry,
Cunningham Kathryn A,
Dineley Kelly T
Publication year - 2018
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1111/adb.12471
Subject(s) - craving , cue reactivity , agonism , abstinence , psychology , addiction , reactivity (psychology) , antagonist , cocaine dependence , self administration , neuroscience , pharmacology , medicine , receptor , psychiatry , alternative medicine , law , pathology , politics , political science
Abstract Cocaine use disorder is a chronic relapsing condition characterized by compulsive drug seeking and taking even after prolonged abstinence periods. Subsequent exposure to drug‐associated cues can promote intense craving and lead to relapse in abstinent humans and rodent models. The responsiveness to these cocaine‐related cues, or ‘cue reactivity’, can trigger relapse and cocaine‐seeking behaviors; cue reactivity is measurable in cocaine‐dependent humans as well as rodent models. Cue reactivity is thought to be predictive of cocaine craving and relapse. Here we report that PPARγ agonism during abstinence from cocaine self‐administration reduced previously active lever pressing in Sprague Dawley rats during cue‐reactivity tests, while administration of the PPARγ antagonist, GW9662, reversed this effect. PPARγ agonism also normalized nuclear ERK activity in the medial prefrontal cortex and hippocampus which was reversed with GW9662. Our results support the utility of PPARγ agonism as a relapse prevention strategy to maintain abstinence in the presence of cocaine‐associated cues.