Ethanol-conditioned place preference is reduced in dopamine D2 receptor-deficient mice

Christopher L. Cunningham, MacKenzie A. Howard, Sylvia J. Gill, Marcelo Rubinstein, Malcolm J. Low, David K. Grandy

Research output: Contribution to journalArticlepeer-review

111 Scopus citations


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/6 × DBA/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.

Original languageEnglish (US)
Pages (from-to)693-699
Number of pages7
JournalPharmacology Biochemistry and Behavior
Issue number4
StatePublished - 2000
Externally publishedYes


  • C57BL/6×DBA/2 F2 hybrid mice
  • Conditioned place preference
  • Dopamine D2 receptor
  • Ethanol
  • Knockout mice
  • Locomotor activity

ASJC Scopus subject areas

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience


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