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The galanin receptor agonist, galnon, attenuates cocaine‐induced reinstatement and dopamine overflow in the frontal cortex
Author(s) -
Ogbonmwan Yvonne E.,
Sciolino Natale R.,
GrovesChapman Jessica L.,
Freeman Kimberly G.,
Schroeder Jason P.,
Edwards Gaylen L.,
Holmes Philip V.,
Weinshenker David
Publication year - 2015
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.12166
Subject(s) - galanin , nucleus accumbens , galanin receptor , agonist , dopamine , self administration , pharmacology , psychology , addiction , cocaine dependence , neuroscience , neuropeptide , receptor , medicine
Relapse represents one of the most significant problems in the long‐term treatment of drug addiction. Cocaine blocks plasma membrane monoamine transporters and increases dopamine ( DA ) overflow in the brain, and DA is critical for the motivational and primary reinforcing effects of the drug as well as cocaine‐primed reinstatement of cocaine seeking in rats, a model of relapse. Thus, modulators of the DA system may be effective for the treatment of cocaine dependence. The endogenous neuropeptide galanin inhibits DA transmission, and both galanin and the synthetic galanin receptor agonist, galnon, interfere with some rewarding properties of cocaine. The purpose of this study was to further assess the effects of galnon on cocaine‐induced behaviors and neurochemistry in rats. We found that galnon attenuated cocaine‐induced motor activity, reinstatement and DA overflow in the frontal cortex at a dose that did not reduce baseline motor activity, stable self‐administration of cocaine, baseline extracellular DA levels or cocaine‐induced DA overflow in the nucleus accumbens (NAc). Similar to cocaine, galnon had no effect on stable food self‐administration but reduced food‐primed reinstatement. These results indicate that galnon can diminish cocaine‐induced hyperactivity and relapse‐like behavior, possibly in part by modulating DA transmission in the frontal cortex.