CHOLECYSTOKININ DOPAMINE INTERACTIONS WITHIN THE NUCLEUS-ACCUMBENS INTHE CONTROL OVER BEHAVIOR BY CONDITIONED REINFORCEMENT

Citation
Gd. Phillips et al., CHOLECYSTOKININ DOPAMINE INTERACTIONS WITHIN THE NUCLEUS-ACCUMBENS INTHE CONTROL OVER BEHAVIOR BY CONDITIONED REINFORCEMENT, Behavioural brain research, 55(2), 1993, pp. 223-231
Citations number
54
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01664328
Volume
55
Issue
2
Year of publication
1993
Pages
223 - 231
Database
ISI
SICI code
0166-4328(1993)55:2<223:CDIWTN>2.0.ZU;2-0
Abstract
Cholecystokinin (CCK) is colocalised with dopamine in the postero-medi al nucleus accumbens (NAS). We have utilised an acquisition of a new r esponse procedure to investigate the interaction between CCK and dopam ine in the control over behaviour by conditioned reinforcers. A condit ioned reinforcer (CR) may be defined as an initially neutral stimulus which gains control over behaviour through selective association with a primary reinforcer. Here, rats learned to associate a light/noise co mpound stimulus with the imminent availability of 10% sucrose reinforc ement. Later, in the absence of sucrose, responding on one of two nove l levers (the CR lever) was acquired and maintained by contingent pres entation of the CR alone, while responding on the second lever had no programmed consequences. In Expt. 1, infusion of 10 mug D-amphetamine within the postero-medial NAS enhanced responding selectively on the C R lever. Infusion of sulphated CCK octapeptide (CCK: 1 or 10 ng) alone within the same area had no effect on response rate. However, infusio n of CCK immediately prior to D-amphetamine caused a dose-dependent po tentiation of the impact Of D-amphetamine upon rates of response on th e CR lever. In Expt. 2, infusion Of D-amphetamine (10 mug) within the postero-medial NAS again enhanced responding selectively upon the CR l ever. Intra-accumbens infusion of CCK (10 ng), or s.c. administration of the CCK(A) receptor antagonist devazepide had no effect upon respon se rates. However, CCK again potentiated the D-amphetamine-induced inc rease in rates of response, and this potentiation was blocked by pretr eatment with devazepide. These results are discussed in terms of the c o-modulation by CCK and dopamine of the processing of reward-related s timuli within the NAS.