All procedures were approved by the National Institute of Mental Health Animal Care and Use Committee and followed the NIH Guidelines ‘Using Animals in Intramural Research.’ Sdy is an autosomal recessive coat mutation that occurred spontaneously in the inbred DBA/2J strain in 1983 at The Jackson Laboratory. The mutation present in our mice was transferred to the C57BL/6J (B6) genetic background by 11 generations of backcrossing into B6 at The Jackson Laboratory and National Institute of Mental Health. The purpose of this backcrossing procedure was to remove the effects on behavior and DA function of the native sdy mouse background strain (DBA/2J), which has been shown to have abnormal behavioral phenotypes referable to the DA system.29 (link) In particular, previous reports have shown that on the DBA/2J genetic background, sdy mice exhibit strong locomotor activity and coordination deficits, as demonstrated by poor performance in the rotarod test and even death during a forced swimming test.30 (link) Also, DBA/2J mice are impaired in θ burst long-term potentiation, in aspects of learning and memory, have higher dopaminergic activity in the forebrain, and are homozygous for four other mutations (cadherin, glycoprotein, tyrosinase-related protein 1 and hemolytic complement) compared with B6 mice.29 (link),31 (link),32 (link) Therefore, the role of the dysbindin mutation is potentially confounded when studied on the DBA/2J genetic background.1 ,23 (link) In these experiments, we used male littermates that were dysbindin-1 null mutant (dys–/–), heterozygous (dys+/–), and wild-type (dys+/+) bred by a heterozygous (dys+/– × dys+/–) mating strategy. Genotypes were identified by PCR analysis of tail DNA (for details see Supplementary Information and Supplementary Figure 10).