PMID:11166059

Citation	Cunningham, CL, Howard, MA, Gill, SJ, Rubinstein, M, Low, MJ and Grandy, DK (2000) Ethanol-conditioned place preference is reduced in dopamine D2 receptor-deficient mice. Pharmacol. Biochem. Behav. 67:693-9
Abstract	Pharmacological blockade studies have supported a role of the dopamine system in ethanol reward for many years, but receptor subtype specificity has been difficult to establish. Recently, genetically engineered mice lacking functional dopamine D2 receptors have been shown to drink less ethanol in a two-bottle choice task. To determine whether reduced ethanol intake reflects a reduction in ethanol reward, D2 receptor-deficient [knockout (KO)] mice were compared to heterozygous (HET) and wild-type (WT; C57BL/6xDBA/2 F2 hybrid) mice in a place conditioning task. Under conditions that produced reliable place preference in both WT and HET mice, KO mice showed no evidence of place conditioning, suggesting that D2 receptor gene inactivation reduced ethanol reward or the ability to learn about ethanol reward. Consistent with previous findings, this mutation also produced a gene dose-related reduction in basal activity levels. Moreover, KO and HET mice showed enhancement of ethanol-stimulated activity relative to WT mice. However, differences in basal and ethanol-stimulated activity did not explain the differences in place conditioning. Overall, this study strongly supports the conclusion that dopamine D2 receptors normally influence ethanol reward in mice.
Links	PubMed
Keywords	Animals; Central Nervous System Depressants/pharmacology; Conditioning (Psychology)/drug effects; Conditioning (Psychology)/physiology; Ethanol/pharmacology; Female; Genotype; Male; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Mice, Knockout; Receptors, Dopamine D2/deficiency; Receptors, Dopamine D2/genetics
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Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
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