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Systemic or intra‐amygdala injections of glucose facilitate memory consolidation for extinction of drug‐induced conditioned reward
Author(s) -
Schroeder Jason P.,
Packard Mark G.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02578.x
Subject(s) - amygdala , extinction (optical mineralogy) , basolateral amygdala , memory consolidation , conditioned place preference , psychology , neuroscience , drug , addiction , pharmacology , medicine , hippocampus , chemistry , mineralogy
The conditioned place preference (CPP) task has been used extensively to investigate the neurobiological bases of drug‐induced reward. The initial expression of a CPP involves memory for an association between environmental stimuli and the affective state produced by a rewarding treatment. The present experiments examined the hypothesis that post‐trial administration of glucose can facilitate memory consolidation processes underlying the extinction of drug‐induced CPP behaviour. Adult male Long‐Evans rats acquired an amphetamine CPP, and subsequently received extinction training. Immediately following extinction training, separate groups of rats received peripheral (100 mg/kg, 500 mg/kg, or 2 g/kg) or intra‐amygdala (basolateral nucleus; 1.5 µg/0.5 µL or 10 µg/0.5 µL) injections of glucose or vehicle. Peripheral (100 mg/kg and 2 g/kg) and intra‐amygdala (1.5 and 10 µg) glucose injections facilitated the extinction of amphetamine CPP behaviour relative to vehicle‐injected controls. Postextinction trial peripheral or intra amygdala glucose injections that were delayed 2 h had no effect. The findings indicate that: (i) extinction of approach behaviour to drug‐associated cues involves the formation of new memories that undergo a time‐dependent consolidation process; and (ii), systemic or intra‐amygdala administration of a known memory‐enhancing agent facilitates extinction of drug‐induced CPP behaviour.