학술논문
Role of dopamine D.sub.1-like and D.sub.2-like receptors in the activation of ingestive behaviour in thirsty rats licking for water
Original Investigation
Original Investigation
Document Type
Academic Journal
Source
Psychopharmacology. December 2019, Vol. 236 Issue 12, p3497, 16 p.
Subject
Language
English
ISSN
0033-3158
Abstract
Author(s): Paolo S. D'Aquila [sup.1], Domenico Elia [sup.1], Adriana Galistu [sup.1] Author Affiliations: (1) grid.11450.31, 0000 0001 2097 9138, Dipartimento di Scienze Biomediche, Università di Sassari, , Viale San Pietro [...]
Rationale Analysis of lick pattern for sucrose and NaCl and of the forced swimming response after dopamine antagonist administration led us to suggest that dopamine on D.sub.1-like receptors is involved in behavioural activation, and the level of activation is 'reboosted' on the basis of an evaluation process involving D.sub.2-like receptors. Although some studies investigated licking microstructure for water after dopamine antagonists, the within-session time course of their effect was never investigated. Objectives The aims of this study were to further investigate the role of dopamine receptors in the mechanisms governing water ingestion, focussing on the within-session time course of the microstructure parameters, and to test the proposed hypothesis. Materials and methods The effects of the dopamine D.sub.1-like receptor antagonist SCH 23390 (0.01-0.04 mg/kg) and of the dopamine D.sub.2-like receptor antagonist raclopride (0.025-0.25 mg/kg) on licking microstructure for water were examined in 20-h water-deprived rats in 30-min sessions. Results As previously observed with sucrose and NaCl, SCH 23390 reduced licking by reducing burst number, suggesting reduced behavioural activation. Moreover, it resulted in an increased burst size. Raclopride reduced the size of licking bursts, while their number was either increased or decreased depending on the dose. Conclusion The results support the suggestion that D.sub.1 receptors are involved in behavioural activation and D.sub.2 receptors are involved in a related evaluation process. Within the framework of the proposed hypothesis, the increased burst size after D.sub.1-like receptor blockade might be interpreted as a pro-hedonic effect consequent to the increased cost of the activation of the licking response.
Rationale Analysis of lick pattern for sucrose and NaCl and of the forced swimming response after dopamine antagonist administration led us to suggest that dopamine on D.sub.1-like receptors is involved in behavioural activation, and the level of activation is 'reboosted' on the basis of an evaluation process involving D.sub.2-like receptors. Although some studies investigated licking microstructure for water after dopamine antagonists, the within-session time course of their effect was never investigated. Objectives The aims of this study were to further investigate the role of dopamine receptors in the mechanisms governing water ingestion, focussing on the within-session time course of the microstructure parameters, and to test the proposed hypothesis. Materials and methods The effects of the dopamine D.sub.1-like receptor antagonist SCH 23390 (0.01-0.04 mg/kg) and of the dopamine D.sub.2-like receptor antagonist raclopride (0.025-0.25 mg/kg) on licking microstructure for water were examined in 20-h water-deprived rats in 30-min sessions. Results As previously observed with sucrose and NaCl, SCH 23390 reduced licking by reducing burst number, suggesting reduced behavioural activation. Moreover, it resulted in an increased burst size. Raclopride reduced the size of licking bursts, while their number was either increased or decreased depending on the dose. Conclusion The results support the suggestion that D.sub.1 receptors are involved in behavioural activation and D.sub.2 receptors are involved in a related evaluation process. Within the framework of the proposed hypothesis, the increased burst size after D.sub.1-like receptor blockade might be interpreted as a pro-hedonic effect consequent to the increased cost of the activation of the licking response.